id: P31749 gene_symbol: AKT1 product_type: PROTEIN status: COMPLETE taxon: id: NCBITaxon:9606 label: Homo sapiens description: 'AKT1 encodes RAC-alpha serine/threonine-protein kinase, a central AGC-family kinase in PI3K-AKT signaling. Its core function is phosphoinositide-regulated protein serine/threonine phosphorylation downstream of growth factor, insulin, and other receptor inputs, with broad downstream effects on mTOR signaling, metabolism, survival, growth, and migration.' alternative_products: - name: '1' id: P31749-1 - name: '2' id: P31749-2 sequence_note: VSP_056180 existing_annotations: - term: id: GO:0005737 label: cytoplasm evidence_type: IBA original_reference_id: GO_REF:0000033 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IBA original_reference_id: GO_REF:0000033 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. The AKT1 kinase domain has been crystallized with small-molecule ATP-competitive inhibitors (PDB 3CQU, 3CQW; 3CQW also contains Mn), confirming the kinase active site/ATP pocket. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - reference_id: PMID:18456494 supporting_text: Akt kinase are explored. X-ray co-crystal structures of two lead series results - term: id: GO:0035556 label: intracellular signal transduction evidence_type: IBA original_reference_id: GO_REF:0000033 review: summary: intracellular signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043066 label: negative regulation of apoptotic process evidence_type: IBA original_reference_id: GO_REF:0000033 review: summary: negative regulation of apoptotic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0008286 label: insulin receptor signaling pathway evidence_type: IBA original_reference_id: GO_REF:0000033 review: summary: insulin receptor signaling pathway is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043536 label: positive regulation of blood vessel endothelial cell migration evidence_type: IBA original_reference_id: GO_REF:0000033 review: summary: positive regulation of blood vessel endothelial cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004672 label: protein kinase activity evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: protein kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005524 label: ATP binding evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: ATP binding is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. The AKT1 kinase domain has been crystallized with small-molecule ATP-competitive inhibitors bound in the ATP pocket (PDB 3CQU, 3CQW; 3CQW also contains Mn), structurally confirming the nucleotide-binding site of the kinase domain. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - reference_id: PMID:18456494 supporting_text: Akt kinase are explored. X-ray co-crystal structures of two lead series results - term: id: GO:0005634 label: nucleus evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: nucleus is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005737 label: cytoplasm evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005758 label: mitochondrial intermembrane space evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: mitochondrial intermembrane space is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030335 label: positive regulation of cell migration evidence_type: IEA original_reference_id: GO_REF:0000117 review: summary: positive regulation of cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0098794 label: postsynapse evidence_type: IEA original_reference_id: GO_REF:0000108 review: summary: postsynapse is retained as a weak database-supported localization/context annotation, but it is not AKT1's core molecular function. action: KEEP_AS_NON_CORE reason: UniProt carries a postsynapse GO cross-reference for AKT1, but the central curatable function remains PI3K-regulated protein serine/threonine phosphorylation rather than a postsynaptic localization claim. supported_by: - reference_id: file:human/AKT1/AKT1-uniprot.txt supporting_text: DR GO; GO:0098794; C:postsynapse; IEA:GOC. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:10102273 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:11154276 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:11438723 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:11839802 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:12176997 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:12244133 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16044149 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16280327 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16282323 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16525023 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16537421 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:17006541 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:17577629 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:17932490 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18191226 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18292230 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18505846 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18562279 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18624398 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18650932 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:18786403 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19122674 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19166854 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19197339 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19541650 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19698782 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20059950 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20186153 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20650008 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20856200 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:21044950 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:21151116 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:21621563 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:21658387 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:21775285 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:22309289 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:22510990 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23010592 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23397142 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23434580 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23693014 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:24291004 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:24412244 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:24658140 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:24670654 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:25241761 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:25910212 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:26256536 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:26871637 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:28514442 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:29997244 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:31515488 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:31980649 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:32296183 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:32814053 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:33961781 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:34591612 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:35271311 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:35512704 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:36126419 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0042802 label: identical protein binding evidence_type: IPI original_reference_id: PMID:17554339 review: summary: identical protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0042802 label: identical protein binding evidence_type: IPI original_reference_id: PMID:35512704 review: summary: identical protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0042802 label: identical protein binding evidence_type: IPI original_reference_id: PMID:7891724 review: summary: identical protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005739 label: mitochondrion evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: mitochondrion is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005819 label: spindle evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: spindle is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005911 label: cell-cell junction evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: cell-cell junction is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0008286 label: insulin receptor signaling pathway evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: insulin receptor signaling pathway is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0009408 label: response to heat evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: response to heat is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0009725 label: response to hormone evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: response to hormone is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010628 label: positive regulation of gene expression evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: positive regulation of gene expression is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010629 label: negative regulation of gene expression evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: negative regulation of gene expression is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010975 label: regulation of neuron projection development evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: regulation of neuron projection development is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0016301 label: kinase activity evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0019901 label: protein kinase binding evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: protein kinase binding is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0036064 label: ciliary basal body evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: ciliary basal body is retained as a database-supported localization/context annotation, but it is not AKT1's core molecular function. action: KEEP_AS_NON_CORE reason: UniProt carries an HPA-supported ciliary basal body GO cross-reference for AKT1. This should be non-core because AKT1's principal function is PI3K-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-uniprot.txt supporting_text: DR GO; GO:0036064; C:ciliary basal body; IDA:HPA. - term: id: GO:0042981 label: regulation of apoptotic process evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: regulation of apoptotic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043066 label: negative regulation of apoptotic process evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: negative regulation of apoptotic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0048009 label: insulin-like growth factor receptor signaling pathway evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: insulin-like growth factor receptor signaling pathway is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0048266 label: behavioral response to pain evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: behavioral response to pain is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0071364 label: cellular response to epidermal growth factor stimulus evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: cellular response to epidermal growth factor stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0090201 label: negative regulation of release of cytochrome c from mitochondria evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: negative regulation of release of cytochrome c from mitochondria is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0098978 label: glutamatergic synapse evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: glutamatergic synapse is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0099175 label: regulation of postsynapse organization evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: regulation of postsynapse organization is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0106310 label: protein serine kinase activity evidence_type: IEA original_reference_id: GO_REF:0000120 review: summary: protein serine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1903898 label: negative regulation of PERK-mediated unfolded protein response evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: negative regulation of PERK-mediated unfolded protein response is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904515 label: positive regulation of TORC2 signaling evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: positive regulation of TORC2 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:2000010 label: positive regulation of protein localization to cell surface evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: positive regulation of protein localization to cell surface is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:2001243 label: negative regulation of intrinsic apoptotic signaling pathway evidence_type: IEA original_reference_id: GO_REF:0000107 review: summary: negative regulation of intrinsic apoptotic signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0042307 label: positive regulation of protein import into nucleus evidence_type: IMP original_reference_id: PMID:16280327 review: summary: positive regulation of protein import into nucleus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: IDA original_reference_id: GO_REF:0000052 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0019221 label: cytokine-mediated signaling pathway evidence_type: TAS original_reference_id: Reactome:R-HSA-9607240 review: summary: cytokine-mediated signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0031295 label: T cell costimulation evidence_type: TAS original_reference_id: Reactome:R-HSA-389356 review: summary: T cell costimulation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0033554 label: cellular response to stress evidence_type: TAS original_reference_id: Reactome:R-HSA-2262752 review: summary: cellular response to stress is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043488 label: regulation of mRNA stability evidence_type: TAS original_reference_id: Reactome:R-HSA-450385 review: summary: regulation of mRNA stability is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043488 label: regulation of mRNA stability evidence_type: TAS original_reference_id: Reactome:R-HSA-450604 review: summary: regulation of mRNA stability is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-198599 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-198609 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-198611 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-198613 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-198621 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-199298 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-199299 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-199839 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-199863 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-200143 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: TAS original_reference_id: Reactome:R-HSA-8948757 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0045746 label: negative regulation of Notch signaling pathway evidence_type: TAS original_reference_id: Reactome:R-HSA-9604328 review: summary: negative regulation of Notch signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0046209 label: nitric oxide metabolic process evidence_type: TAS original_reference_id: Reactome:R-HSA-203615 review: summary: nitric oxide metabolic process is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0097700 label: vascular endothelial cell response to laminar fluid shear stress evidence_type: TAS original_reference_id: Reactome:R-HSA-9856530 review: summary: vascular endothelial cell response to laminar fluid shear stress is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1901796 label: regulation of signal transduction by p53 class mediator evidence_type: TAS original_reference_id: Reactome:R-HSA-6804758 review: summary: regulation of signal transduction by p53 class mediator is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1901796 label: regulation of signal transduction by p53 class mediator evidence_type: TAS original_reference_id: Reactome:R-HSA-6804759 review: summary: regulation of signal transduction by p53 class mediator is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:2000074 label: regulation of type B pancreatic cell development evidence_type: TAS original_reference_id: Reactome:R-HSA-211163 review: summary: regulation of type B pancreatic cell development is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: EXP original_reference_id: PMID:10376603 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: EXP original_reference_id: PMID:17030608 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-1358791 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-198599 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-198609 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-198611 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-198613 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-198621 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-199298 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-199299 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-199839 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-199863 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-200143 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-211164 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399941 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399966 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399969 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399977 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399981 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399982 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399985 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399988 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399992 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399996 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2399999 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-2400001 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-3769394 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-377186 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-389756 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-432110 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-6805640 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-6805785 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-8933446 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-8948757 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-9624526 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-9699579 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-NUL-3139045 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: Reactome:R-NUL-8939977 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: IDA original_reference_id: PMID:40285646 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IDA original_reference_id: PMID:40285646 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0051897 label: positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IDA original_reference_id: PMID:40285646 review: summary: positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0106310 label: protein serine kinase activity evidence_type: IDA original_reference_id: PMID:23431171 review: summary: protein serine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IDA original_reference_id: PMID:28147277 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0008286 label: insulin receptor signaling pathway evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: insulin receptor signaling pathway is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: NAS original_reference_id: PMID:21711983 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0160213 label: beta-arrestin-dependent dopamine receptor signaling pathway evidence_type: NAS original_reference_id: PMID:21711983 review: summary: beta-arrestin-dependent dopamine receptor signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0002430 label: complement receptor mediated signaling pathway evidence_type: IDA original_reference_id: PMID:19162005 review: summary: complement receptor mediated signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004712 label: protein serine/threonine/tyrosine kinase activity evidence_type: IDA original_reference_id: PMID:19162005 review: summary: protein serine/threonine/tyrosine kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IDA original_reference_id: PMID:19162005 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:29343641 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1905786 label: positive regulation of anaphase-promoting complex-dependent catabolic process evidence_type: IDA original_reference_id: PMID:29343641 review: summary: positive regulation of anaphase-promoting complex-dependent catabolic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: PMID:21711983 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0007173 label: epidermal growth factor receptor signaling pathway evidence_type: IMP original_reference_id: PMID:18483258 review: summary: epidermal growth factor receptor signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0019900 label: kinase binding evidence_type: IPI original_reference_id: PMID:21177249 review: summary: kinase binding is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030335 label: positive regulation of cell migration evidence_type: IMP original_reference_id: PMID:21177249 review: summary: positive regulation of cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IMP original_reference_id: PMID:18483258 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IMP original_reference_id: PMID:9373175 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0045944 label: positive regulation of transcription by RNA polymerase II evidence_type: IDA original_reference_id: PMID:19057511 review: summary: positive regulation of transcription by RNA polymerase II is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1900087 label: positive regulation of G1/S transition of mitotic cell cycle evidence_type: IMP original_reference_id: PMID:18483258 review: summary: positive regulation of G1/S transition of mitotic cell cycle is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1903384 label: negative regulation of hydrogen peroxide-induced neuron intrinsic apoptotic signaling pathway evidence_type: IMP original_reference_id: PMID:21177249 review: summary: negative regulation of hydrogen peroxide-induced neuron intrinsic apoptotic signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904841 label: TORC2 complex binding evidence_type: IDA original_reference_id: PMID:21177249 review: summary: TORC2 complex binding is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0160049 label: negative regulation of cGAS/STING signaling pathway evidence_type: IDA original_reference_id: PMID:12172553 review: summary: negative regulation of cGAS/STING signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1903898 label: negative regulation of PERK-mediated unfolded protein response evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: negative regulation of PERK-mediated unfolded protein response is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0001649 label: osteoblast differentiation evidence_type: IDA original_reference_id: PMID:22869525 review: summary: osteoblast differentiation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032991 label: protein-containing complex evidence_type: IDA original_reference_id: PMID:23223530 review: summary: protein-containing complex is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IMP original_reference_id: PMID:19573808 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:30504268 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005758 label: mitochondrial intermembrane space evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: mitochondrial intermembrane space is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0072752 label: cellular response to rapamycin evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: cellular response to rapamycin is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1903318 label: negative regulation of protein maturation evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: negative regulation of protein maturation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0106310 label: protein serine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-9860792 review: summary: protein serine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:8524413 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030335 label: positive regulation of cell migration evidence_type: IDA original_reference_id: PMID:38020884 review: summary: positive regulation of cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-9841244 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-9841265 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0106310 label: protein serine kinase activity evidence_type: TAS original_reference_id: Reactome:R-HSA-9841265 review: summary: protein serine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0160049 label: negative regulation of cGAS/STING signaling pathway evidence_type: IDA original_reference_id: PMID:26440888 review: summary: negative regulation of cGAS/STING signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IDA original_reference_id: PMID:21321938 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004672 label: protein kinase activity evidence_type: IDA original_reference_id: PMID:31204173 review: summary: protein kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1902018 label: negative regulation of cilium assembly evidence_type: IDA original_reference_id: PMID:31204173 review: summary: negative regulation of cilium assembly is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:30514904 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0071364 label: cellular response to epidermal growth factor stimulus evidence_type: IDA original_reference_id: PMID:30514904 review: summary: cellular response to epidermal growth factor stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904263 label: positive regulation of TORC1 signaling evidence_type: IDA original_reference_id: PMID:30514904 review: summary: positive regulation of TORC1 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:24529379 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032869 label: cellular response to insulin stimulus evidence_type: IDA original_reference_id: PMID:24529379 review: summary: cellular response to insulin stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0150033 label: negative regulation of protein localization to lysosome evidence_type: IDA original_reference_id: PMID:24529379 review: summary: negative regulation of protein localization to lysosome is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904263 label: positive regulation of TORC1 signaling evidence_type: IDA original_reference_id: PMID:24529379 review: summary: positive regulation of TORC1 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:12172553 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0016020 label: membrane evidence_type: IDA original_reference_id: PMID:24529379 review: summary: membrane is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032869 label: cellular response to insulin stimulus evidence_type: IDA original_reference_id: PMID:12172553 review: summary: cellular response to insulin stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904263 label: positive regulation of TORC1 signaling evidence_type: IDA original_reference_id: PMID:12172553 review: summary: positive regulation of TORC1 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:17386266 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032869 label: cellular response to insulin stimulus evidence_type: IDA original_reference_id: PMID:17386266 review: summary: cellular response to insulin stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904263 label: positive regulation of TORC1 signaling evidence_type: IDA original_reference_id: PMID:17386266 review: summary: positive regulation of TORC1 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:31548394 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904263 label: positive regulation of TORC1 signaling evidence_type: IDA original_reference_id: PMID:31548394 review: summary: positive regulation of TORC1 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:23512198 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032436 label: positive regulation of proteasomal ubiquitin-dependent protein catabolic process evidence_type: IDA original_reference_id: PMID:23512198 review: summary: AKT1 phosphorylation of Rac1 promotes FBXL19-mediated Rac1 ubiquitination and degradation, supporting this proteasomal catabolic context but not making proteasome regulation a core AKT1 function. action: KEEP_AS_NON_CORE reason: Keep as non-core because the evidence is substrate-specific regulation downstream of AKT1 kinase activity, not a general role as proteasome machinery. supported_by: - reference_id: PMID:23512198 supporting_text: Protein kinase AKT-mediated phosphorylation of Rac1 at serine(71) was essential for FBXL19-mediated Rac1 ubiquitination. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:15861136 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0110002 label: regulation of tRNA methylation evidence_type: IDA original_reference_id: PMID:15861136 review: summary: regulation of tRNA methylation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005938 label: cell cortex evidence_type: NAS original_reference_id: PMID:19126672 review: summary: cell cortex is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010748 label: negative regulation of long-chain fatty acid import across plasma membrane evidence_type: IMP original_reference_id: PMID:16814735 review: summary: negative regulation of long-chain fatty acid import across plasma membrane is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010907 label: positive regulation of glucose metabolic process evidence_type: IMP original_reference_id: PMID:16814735 review: summary: positive regulation of glucose metabolic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030291 label: protein serine/threonine kinase inhibitor activity evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: protein serine/threonine kinase inhibitor activity is not a supported direct molecular activity for AKT1. action: REMOVE reason: AKT1 acts as a protein serine/threonine kinase and signaling effector; this annotation reverses or overextends the direction of regulation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030291 label: protein serine/threonine kinase inhibitor activity evidence_type: TAS original_reference_id: PMID:21711983 review: summary: protein serine/threonine kinase inhibitor activity is not a supported direct molecular activity for AKT1. action: REMOVE reason: AKT1 acts as a protein serine/threonine kinase and signaling effector; this annotation reverses or overextends the direction of regulation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0031999 label: negative regulation of fatty acid beta-oxidation evidence_type: IMP original_reference_id: PMID:16814735 review: summary: negative regulation of fatty acid beta-oxidation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032869 label: cellular response to insulin stimulus evidence_type: IMP original_reference_id: PMID:16814735 review: summary: cellular response to insulin stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0045725 label: positive regulation of glycogen biosynthetic process evidence_type: IMP original_reference_id: PMID:16814735 review: summary: positive regulation of glycogen biosynthetic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0046326 label: positive regulation of D-glucose import across plasma membrane evidence_type: IMP original_reference_id: PMID:16814735 review: summary: positive regulation of D-glucose import across plasma membrane is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:14749367 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005737 label: cytoplasm evidence_type: IDA original_reference_id: PMID:26440888 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:31915252 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:33594058 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1904263 label: positive regulation of TORC1 signaling evidence_type: IDA original_reference_id: PMID:33594058 review: summary: positive regulation of TORC1 signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1905552 label: positive regulation of protein localization to endoplasmic reticulum evidence_type: IDA original_reference_id: PMID:32322062 review: summary: positive regulation of protein localization to endoplasmic reticulum is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:26440888 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:33505021 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0070848 label: response to growth factor evidence_type: IDA original_reference_id: PMID:33505021 review: summary: response to growth factor is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0099104 label: potassium channel activator activity evidence_type: IDA original_reference_id: PMID:33505021 review: summary: potassium channel activator activity is supported as a direct but non-core AKT1 molecular activity involving TMEM175. action: KEEP_AS_NON_CORE reason: UniProt explicitly describes AKT1 as an activator of TMEM175 potassium channel activity in response to growth factors, independently of AKT1 kinase activity. This should be retained as a non-core molecular activity rather than removed. supported_by: - reference_id: file:human/AKT1/AKT1-uniprot.txt supporting_text: | Also acts as an activator of TMEM175 potassium channel activity in response to growth factors: forms the lysoK(GF) complex together with TMEM175 and acts by promoting TMEM175 channel activation, independently of its protein kinase activity. - term: id: GO:0003376 label: sphingosine-1-phosphate receptor signaling pathway evidence_type: IMP original_reference_id: PMID:18558630 review: summary: sphingosine-1-phosphate receptor signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010595 label: positive regulation of endothelial cell migration evidence_type: IMP original_reference_id: PMID:18558630 review: summary: positive regulation of endothelial cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030027 label: lamellipodium evidence_type: NAS original_reference_id: PMID:19126672 review: summary: lamellipodium is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010761 label: fibroblast migration evidence_type: NAS original_reference_id: PMID:19126672 review: summary: fibroblast migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:32322062 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0046889 label: positive regulation of lipid biosynthetic process evidence_type: IDA original_reference_id: PMID:32322062 review: summary: positive regulation of lipid biosynthetic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005516 label: calmodulin binding evidence_type: IDA original_reference_id: PMID:29104511 review: summary: calmodulin binding is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0002042 label: cell migration involved in sprouting angiogenesis evidence_type: IMP original_reference_id: PMID:28341552 review: summary: cell migration involved in sprouting angiogenesis is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010628 label: positive regulation of gene expression evidence_type: IMP original_reference_id: PMID:28341552 review: summary: positive regulation of gene expression is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction evidence_type: IMP original_reference_id: PMID:28341552 review: summary: phosphatidylinositol 3-kinase/protein kinase B signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0140052 label: cellular response to oxidised low-density lipoprotein particle stimulus evidence_type: IMP original_reference_id: PMID:28341552 review: summary: cellular response to oxidised low-density lipoprotein particle stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1903038 label: negative regulation of leukocyte cell-cell adhesion evidence_type: IMP original_reference_id: PMID:28341552 review: summary: negative regulation of leukocyte cell-cell adhesion is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:2000402 label: negative regulation of lymphocyte migration evidence_type: IMP original_reference_id: PMID:28341552 review: summary: negative regulation of lymphocyte migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010628 label: positive regulation of gene expression evidence_type: ISS original_reference_id: PMID:18292230 review: summary: positive regulation of gene expression is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0031397 label: negative regulation of protein ubiquitination evidence_type: IMP original_reference_id: PMID:18292230 review: summary: AKT1 can prevent CHIP-mediated tau ubiquitination and degradation, supporting a substrate-specific protein quality-control context but not a core AKT1 function. action: KEEP_AS_NON_CORE reason: Keep as non-core because the evidence concerns tau/CHIP regulation downstream of AKT1 signaling rather than a general ubiquitination or proteostasis role. supported_by: - reference_id: PMID:18292230 supporting_text: Akt also prevents CHIP-induced tau ubiquitination and its subsequent degradation. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: NAS original_reference_id: PMID:28386764 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23300339 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0060079 label: excitatory postsynaptic potential evidence_type: NAS original_reference_id: PMID:21711983 review: summary: excitatory postsynaptic potential is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:10983986 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:10983986 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0042803 label: protein homodimerization activity evidence_type: IDA original_reference_id: PMID:10983986 review: summary: protein homodimerization activity is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20878056 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0007173 label: epidermal growth factor receptor signaling pathway evidence_type: IDA original_reference_id: PMID:20878056 review: summary: epidermal growth factor receptor signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032991 label: protein-containing complex evidence_type: IDA original_reference_id: PMID:20878056 review: summary: protein-containing complex is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0042981 label: regulation of apoptotic process evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: regulation of apoptotic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0016242 label: negative regulation of macroautophagy evidence_type: NAS original_reference_id: PMID:23778976 review: summary: PI3K-AKT-MTORC1 signaling can suppress autophagy in some contexts, but this paper emphasizes that detachment-induced macroautophagy is cell-context dependent. action: KEEP_AS_NON_CORE reason: Keep as non-core because macroautophagy regulation is a downstream pathway context of AKT1 signaling and not its direct molecular function. supported_by: - reference_id: PMID:23778976 supporting_text: Enforced activation of this pathway is not sufficient to suppress detachment-induced autophagy in MECs. - term: id: GO:0031929 label: TOR signaling evidence_type: NAS original_reference_id: PMID:23778976 review: summary: TOR signaling is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043276 label: anoikis evidence_type: NAS original_reference_id: PMID:23778976 review: summary: anoikis is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23251525 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0035655 label: interleukin-18-mediated signaling pathway evidence_type: IDA original_reference_id: PMID:21321938 review: summary: interleukin-18-mediated signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0048661 label: positive regulation of smooth muscle cell proliferation evidence_type: IDA original_reference_id: PMID:21321938 review: summary: positive regulation of smooth muscle cell proliferation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-8848758 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1900182 label: positive regulation of protein localization to nucleus evidence_type: IMP original_reference_id: PMID:20605787 review: summary: positive regulation of protein localization to nucleus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20605787 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0032079 label: positive regulation of endodeoxyribonuclease activity evidence_type: IDA original_reference_id: PMID:20605787 review: summary: positive regulation of endodeoxyribonuclease activity is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1990090 label: cellular response to nerve growth factor stimulus evidence_type: IMP original_reference_id: PMID:20605787 review: summary: cellular response to nerve growth factor stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0018107 label: peptidyl-threonine phosphorylation evidence_type: IDA original_reference_id: PMID:20605787 review: summary: peptidyl-threonine phosphorylation is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16792529 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0031982 label: vesicle evidence_type: IDA original_reference_id: PMID:16792529 review: summary: vesicle is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:23676467 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0070585 label: protein localization to mitochondrion evidence_type: IMP original_reference_id: PMID:23962723 review: summary: protein localization to mitochondrion is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0072656 label: maintenance of protein location in mitochondrion evidence_type: IMP original_reference_id: PMID:23962723 review: summary: maintenance of protein location in mitochondrion is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0060416 label: response to growth hormone evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: response to growth hormone is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1990418 label: response to insulin-like growth factor stimulus evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: response to insulin-like growth factor stimulus is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20237237 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:24784001 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:25190803 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005737 label: cytoplasm evidence_type: IDA original_reference_id: PMID:25190803 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0006979 label: response to oxidative stress evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: response to oxidative stress is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0071889 label: 14-3-3 protein binding evidence_type: IPI original_reference_id: PMID:10102273 review: summary: 14-3-3 protein binding is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004712 label: protein serine/threonine/tyrosine kinase activity evidence_type: IDA original_reference_id: PMID:22797923 review: summary: protein serine/threonine/tyrosine kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0001938 label: positive regulation of endothelial cell proliferation evidence_type: IMP original_reference_id: PMID:19850054 review: summary: positive regulation of endothelial cell proliferation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1902176 label: negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway evidence_type: NAS original_reference_id: PMID:16604263 review: summary: negative regulation of oxidative stress-induced intrinsic apoptotic signaling pathway is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:2001240 label: negative regulation of extrinsic apoptotic signaling pathway in absence of ligand evidence_type: TAS original_reference_id: PMID:10748004 review: summary: negative regulation of extrinsic apoptotic signaling pathway in absence of ligand is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-2399988 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-2399992 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-2399996 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-2399997 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-2399999 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2219536 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2243942 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399941 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399966 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399969 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399977 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399981 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399982 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399985 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2399997 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2400001 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-2219536 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-2243937 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-2243938 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-2243942 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-199298 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-199299 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-199839 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-199863 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-211164 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-3769394 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-6805640 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-6805785 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-9624526 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-HSA-9699579 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005654 label: nucleoplasm evidence_type: TAS original_reference_id: Reactome:R-NUL-8939977 review: summary: nucleoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-1358791 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-1497784 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-1497796 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-1497810 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-198270 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-198599 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-198609 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-198611 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-198613 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-198621 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-199425 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-200143 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-202111 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-202127 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-202137 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-389756 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-390329 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-450490 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-450499 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-6811504 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-8933446 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-8948757 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-9604328 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-NUL-3139045 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-202111 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-202137 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-377186 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-432110 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-9860759 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-9860792 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-198270 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-198640 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-2317314 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-9860800 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:10102273 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19903888 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010507 label: negative regulation of autophagy evidence_type: IMP original_reference_id: PMID:18387192 review: summary: AKT1 negatively regulates autophagy; more specific CMA regulatory evidence (PMID:26118642) supports a separate GO:1904715 annotation. action: KEEP_AS_NON_CORE reason: Keep the existing broad autophagy annotation as non-core. The PN projection is supported conservatively as a separate proposed GO:1904715 annotation rather than making AKT1 direct CMA machinery or a core proteostasis gene. additional_reference_ids: - PMID:26118642 - file:projects/PROTEOSTASIS/reports/pn_projection/pn_projected_gene_go_summary.tsv supported_by: - reference_id: PMID:18387192 supporting_text: Knockdown of AKT1 resulted in an increase of dNGLUC release from cells expressing Actin-LC3-dNGLUC. - reference_id: PMID:26118642 supporting_text: Overall, these results support an inhibitory effect of Akt1 on CMA. - term: id: GO:0045861 label: negative regulation of proteolysis evidence_type: IMP original_reference_id: PMID:18387192 review: summary: This broad proteolysis term reflects AKT1-mediated autophagy regulation from the reporter assay, but it is less informative than autophagy or CMA regulation. action: KEEP_AS_NON_CORE reason: Keep as non-core and avoid using this broad term as a proteostasis core assignment; AKT1's direct function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: PMID:18387192 supporting_text: Knockdown of AKT1 resulted in an increase of dNGLUC release from cells expressing Actin-LC3-dNGLUC. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2317332 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-2400010 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-6790041 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-8848751 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: TAS original_reference_id: Reactome:R-HSA-9603279 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-199443 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-2317332 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: Reactome:R-HSA-9603279 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19162005 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20682768 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:21333377 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0090201 label: negative regulation of release of cytochrome c from mitochondria evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: negative regulation of release of cytochrome c from mitochondria is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:16540465 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: TAS original_reference_id: PMID:21432781 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005524 label: ATP binding evidence_type: IDA original_reference_id: PMID:16540465 review: summary: ATP binding is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005634 label: nucleus evidence_type: TAS original_reference_id: PMID:21432781 review: summary: nucleus is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005737 label: cytoplasm evidence_type: TAS original_reference_id: PMID:21432781 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: TAS original_reference_id: PMID:21432781 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0007165 label: signal transduction evidence_type: TAS original_reference_id: PMID:21432781 review: summary: signal transduction is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0008283 label: cell population proliferation evidence_type: TAS original_reference_id: PMID:21432781 review: summary: cell population proliferation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030154 label: cell differentiation evidence_type: TAS original_reference_id: PMID:21432781 review: summary: cell differentiation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030334 label: regulation of cell migration evidence_type: TAS original_reference_id: PMID:21432781 review: summary: regulation of cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0060644 label: mammary gland epithelial cell differentiation evidence_type: TAS original_reference_id: PMID:21432781 review: summary: mammary gland epithelial cell differentiation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20086174 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16417524 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030334 label: regulation of cell migration evidence_type: IMP original_reference_id: PMID:19934221 review: summary: regulation of cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:19667065 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0033138 label: positive regulation of peptidyl-serine phosphorylation evidence_type: IDA original_reference_id: PMID:19667065 review: summary: positive regulation of peptidyl-serine phosphorylation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19262695 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:20333297 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005634 label: nucleus evidence_type: IDA original_reference_id: PMID:20333297 review: summary: nucleus is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: IDA original_reference_id: PMID:20333297 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005829 label: cytosol evidence_type: IDA original_reference_id: PMID:21045808 review: summary: cytosol is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:12791994 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043536 label: positive regulation of blood vessel endothelial cell migration evidence_type: IDA original_reference_id: PMID:20011604 review: summary: positive regulation of blood vessel endothelial cell migration is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0010975 label: regulation of neuron projection development evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: regulation of neuron projection development is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:19713527 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:1903078 label: positive regulation of protein localization to plasma membrane evidence_type: IMP original_reference_id: PMID:8940145 review: summary: positive regulation of protein localization to plasma membrane is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0045725 label: positive regulation of glycogen biosynthetic process evidence_type: NAS original_reference_id: PMID:17925406 review: summary: positive regulation of glycogen biosynthetic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005547 label: phosphatidylinositol-3,4,5-trisphosphate binding evidence_type: IDA original_reference_id: PMID:19203586 review: summary: phosphatidylinositol-3,4,5-trisphosphate binding is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005737 label: cytoplasm evidence_type: IDA original_reference_id: PMID:19203586 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: IDA original_reference_id: PMID:19203586 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030307 label: positive regulation of cell growth evidence_type: IDA original_reference_id: PMID:19203586 review: summary: positive regulation of cell growth is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043066 label: negative regulation of apoptotic process evidence_type: IDA original_reference_id: PMID:19203586 review: summary: negative regulation of apoptotic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0043325 label: phosphatidylinositol-3,4-bisphosphate binding evidence_type: IDA original_reference_id: PMID:19203586 review: summary: phosphatidylinositol-3,4-bisphosphate binding is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005979 label: regulation of glycogen biosynthetic process evidence_type: IMP original_reference_id: PMID:8940145 review: summary: regulation of glycogen biosynthetic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0045600 label: positive regulation of fat cell differentiation evidence_type: IMP original_reference_id: PMID:8940145 review: summary: positive regulation of fat cell differentiation is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0046326 label: positive regulation of D-glucose import across plasma membrane evidence_type: IMP original_reference_id: PMID:8940145 review: summary: positive regulation of D-glucose import across plasma membrane is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0046889 label: positive regulation of lipid biosynthetic process evidence_type: IMP original_reference_id: PMID:8940145 review: summary: positive regulation of lipid biosynthetic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0019899 label: enzyme binding evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: enzyme binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0051247 label: positive regulation of protein metabolic process evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: positive regulation of protein metabolic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0070141 label: response to UV-A evidence_type: IDA original_reference_id: PMID:18483258 review: summary: response to UV-A is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0030235 label: nitric-oxide synthase regulator activity evidence_type: IMP original_reference_id: PMID:10376603 review: summary: nitric-oxide synthase regulator activity is supported through Akt-dependent eNOS phosphorylation, but it is not AKT1's core molecular function. action: KEEP_AS_NON_CORE reason: PMID:10376603 directly supports AKT/PKB-mediated eNOS activation by phosphorylation. This should be retained as a non-core regulatory molecular function while the core AKT1 function remains PI3K-regulated protein serine/threonine kinase activity. supported_by: - reference_id: PMID:10376603 supporting_text: Here we demonstrate that the serine/threonine protein kinase Akt/PKB mediates the activation of eNOS, leading to increased NO production. - term: id: GO:0034405 label: response to fluid shear stress evidence_type: IMP original_reference_id: PMID:10376603 review: summary: response to fluid shear stress is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0045429 label: positive regulation of nitric oxide biosynthetic process evidence_type: IMP original_reference_id: PMID:10376603 review: summary: positive regulation of nitric oxide biosynthetic process is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005886 label: plasma membrane evidence_type: IDA original_reference_id: PMID:14749367 review: summary: plasma membrane is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0006468 label: protein phosphorylation evidence_type: IDA original_reference_id: PMID:14749367 review: summary: protein phosphorylation is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0006924 label: activation-induced cell death of T cells evidence_type: IMP original_reference_id: PMID:14749367 review: summary: activation-induced cell death of T cells is a supported pathway, substrate, interaction, localization, or phenotype context for AKT1 but not its core molecular function. action: KEEP_AS_NON_CORE reason: AKT1 has broad downstream effects; this annotation should be retained as context while the core function remains PI3K-regulated protein serine/threonine phosphorylation. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0016301 label: kinase activity evidence_type: IDA original_reference_id: PMID:14749367 review: summary: kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0035556 label: intracellular signal transduction evidence_type: IDA original_reference_id: PMID:14749367 review: summary: intracellular signal transduction is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:16139227 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005515 label: protein binding evidence_type: IPI original_reference_id: PMID:16139227 review: summary: protein binding is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0018105 label: peptidyl-serine phosphorylation evidence_type: IDA original_reference_id: PMID:16139227 review: summary: peptidyl-serine phosphorylation is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005524 label: ATP binding evidence_type: IC original_reference_id: PMID:11994271 review: summary: ATP binding is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004674 label: protein serine/threonine kinase activity evidence_type: IDA original_reference_id: PMID:11994271 review: summary: protein serine/threonine kinase activity is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0005737 label: cytoplasm evidence_type: ISS original_reference_id: GO_REF:0000024 review: summary: cytoplasm is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0006468 label: protein phosphorylation evidence_type: IDA original_reference_id: PMID:11994271 review: summary: protein phosphorylation is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0008286 label: insulin receptor signaling pathway evidence_type: IMP original_reference_id: PMID:8978681 review: summary: insulin receptor signaling pathway is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0048009 label: insulin-like growth factor receptor signaling pathway evidence_type: IMP original_reference_id: PMID:8978681 review: summary: insulin-like growth factor receptor signaling pathway is consistent with AKT1 as a phosphoinositide-regulated serine/threonine kinase in PI3K-AKT signaling. action: ACCEPT reason: Falcon research and UniProt support AKT1 activation downstream of PI3K and phosphorylation of serine/threonine substrates in growth, metabolic, survival, and mTOR-linked signaling. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0004672 label: protein kinase activity evidence_type: TAS original_reference_id: PMID:10570282 review: summary: protein kinase activity is directionally correct but less specific than AKT1's established kinase activity. action: MODIFY reason: AKT1 is specifically a protein serine/threonine kinase; the broader kinase term should be replaced with the more precise GO term. proposed_replacement_terms: - id: GO:0004674 label: protein serine/threonine kinase activity supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0006809 label: nitric oxide biosynthetic process evidence_type: TAS original_reference_id: PMID:10376602 review: summary: nitric oxide biosynthetic process is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0007165 label: signal transduction evidence_type: TAS original_reference_id: PMID:10570282 review: summary: signal transduction is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0007186 label: G protein-coupled receptor signaling pathway evidence_type: TAS original_reference_id: PMID:10570282 review: summary: G protein-coupled receptor signaling pathway is too generic or indirect for AKT1. action: MARK_AS_OVER_ANNOTATED reason: The annotation should not be treated as a core function when the supported molecular activity is phosphoinositide-regulated protein serine/threonine kinase activity. supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - term: id: GO:0009408 label: response to heat evidence_type: TAS original_reference_id: PMID:10958679 review: summary: AKT signaling affects thermosensitivity after severe heat shock, but acquired thermotolerance is primarily Hsp72/JNK driven and is not core AKT1 biology. action: KEEP_AS_NON_CORE reason: Keep as non-core because the evidence supports survival response under heat stress, not a direct chaperone or proteostasis role for AKT1. supported_by: - reference_id: PMID:10958679 supporting_text: Suppression of Akt or ERK1 and -2 kinases increased cell thermosensitivity. - term: id: GO:1904715 label: negative regulation of chaperone-mediated autophagy evidence_type: IMP original_reference_id: PMID:26118642 review: summary: AKT1 negatively regulates chaperone-mediated autophagy through lysosomal TORC2/PHLPP1/Akt control of LAMP-2A translocation-complex dynamics. action: NEW reason: The PN projection to GO:1904715 is more specific than the existing negative regulation of autophagy annotation and is supported by direct CMA assays. Treat this as a non-core regulatory process, not as direct participation in CMA substrate delivery/degradation or as a general proteostasis core function. additional_reference_ids: - file:projects/PROTEOSTASIS/reports/pn_projection/pn_projected_gene_go_summary.tsv - file:projects/PROTEOSTASIS/mappings/autophagy_lysosome_pathway.yaml supported_by: - reference_id: PMID:26118642 supporting_text: Overall, these results support an inhibitory effect of Akt1 on CMA. - reference_id: PMID:26118642 supporting_text: Inhibition of Akt activity in isolated lysosomes lead to a similar dose-dependent increase in the amount of CMA translocation complex. - reference_id: file:projects/PROTEOSTASIS/reports/pn_projection/pn_projected_gene_go_summary.tsv supporting_text: AKT1 GO:1904715 negative regulation of chaperone-mediated autophagy more_specific_than_existing_goa. references: - id: GO_REF:0000024 title: 'Manual transfer of experimentally-verified manual GO annotation data to orthologs by curator judgment of sequence similarity' findings: [] - id: GO_REF:0000033 title: 'Annotation inferences using phylogenetic trees' findings: [] - id: GO_REF:0000052 title: 'Gene Ontology annotation based on curation of immunofluorescence data' findings: [] - id: GO_REF:0000107 title: 'Automatic transfer of experimentally verified manual GO annotation data to orthologs using Ensembl Compara' findings: [] - id: GO_REF:0000108 title: 'Automatic assignment of GO terms using logical inference, based on inter-ontology links' findings: [] - id: GO_REF:0000117 title: 'Electronic Gene Ontology annotations created by ARBA machine learning models' findings: [] - id: GO_REF:0000120 title: 'Combined Automated Annotation using Multiple IEA Methods' findings: [] - id: PMID:10102273 title: 'Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor.' findings: [] - id: PMID:10376602 title: 'Regulation of endothelium-derived nitric oxide production by the protein kinase Akt.' findings: [] - id: PMID:10376603 title: 'Activation of nitric oxide synthase in endothelial cells by Akt-dependent phosphorylation.' findings: [] - id: PMID:10570282 title: 'The CXC chemokine stromal cell-derived factor activates a Gi-coupled phosphoinositide 3-kinase in T lymphocytes.' findings: [] - id: PMID:10748004 title: 'A phosphatidylinositol 3-kinase/Akt pathway, activated by tumor necrosis factor or interleukin-1, inhibits apoptosis but does not activate NFkappaB in human endothelial cells.' findings: [] - id: PMID:10958679 title: 'Hsp72-mediated suppression of c-Jun N-terminal kinase is implicated in development of tolerance to caspase-independent cell death.' findings: [] - id: PMID:10983986 title: 'The protooncogene TCL1 is an Akt kinase coactivator.' findings: [] - id: PMID:11154276 title: 'Akt phosphorylates and negatively regulates apoptosis signal-regulating kinase 1.' findings: [] - id: PMID:11438723 title: 'Visualization of biochemical networks in living cells.' findings: [] - id: PMID:11839802 title: 'Integrin alpha 2 beta 1 promotes activation of protein phosphatase 2A and dephosphorylation of Akt and glycogen synthase kinase 3 beta.' findings: [] - id: PMID:11994271 title: 'A method to identify serine kinase substrates. Akt phosphorylates a novel adipocyte protein with a Rab GTPase-activating protein (GAP) domain.' findings: [] - id: PMID:12172553 title: 'TSC2 is phosphorylated and inhibited by Akt and suppresses mTOR signalling.' findings: [] - id: PMID:12176997 title: 'Akt forms an intracellular complex with heat shock protein 90 (Hsp90) and Cdc37 and is destabilized by inhibitors of Hsp90 function.' findings: [] - id: PMID:12244133 title: 'Binding of protein kinase B to the plakin family member periplakin.' findings: [] - id: PMID:12791994 title: 'TRB3: a tribbles homolog that inhibits Akt/PKB activation by insulin in liver.' findings: [] - id: PMID:14749367 title: 'Regulation of apoptosis by the Ft1 protein, a new modulator of protein kinase B/Akt.' findings: [] - id: PMID:15861136 title: 'The tRNA methylase METTL1 is phosphorylated and inactivated by PKB and RSK in vitro and in cells.' findings: [] - id: PMID:16044149 title: 'Activation of the protein kinase B pathway by the HPV-16 E7 oncoprotein occurs through a mechanism involving interaction with PP2A.' findings: [] - id: PMID:16139227 title: 'Akt/PKB regulates actin organization and cell motility via Girdin/APE.' findings: [] - id: PMID:16280327 title: 'A pathway for tumor necrosis factor-alpha-induced Bcl10 nuclear translocation. Bcl10 is up-regulated by NF-kappaB and phosphorylated by Akt1 and then complexes with Bcl3 to enter the nucleus.' findings: [] - id: PMID:16282323 title: 'Evidence that Ser87 of BimEL is phosphorylated by Akt and regulates BimEL apoptotic function.' findings: [] - id: PMID:16417524 title: 'Akt phosphorylates and suppresses the transactivation of retinoic acid receptor alpha.' findings: [] - id: PMID:16525023 title: 'Akt binds to and phosphorylates phospholipase C-gamma1 in response to epidermal growth factor.' findings: [] - id: PMID:16537421 title: 'Infection of human cancer cells with myxoma virus requires Akt activation via interaction with a viral ankyrin-repeat host range factor.' findings: [] - id: PMID:16540465 title: 'Kinetic mechanism of AKT/PKB enzyme family.' findings: [] - id: PMID:16604263 title: 'Neuroprotection of insulin against oxidative stress-induced apoptosis in cultured retinal neurons: involvement of phosphoinositide 3-kinase/Akt signal pathway.' findings: [] - id: PMID:16792529 title: 'A WD-FYVE protein binds to the kinases Akt and PKCzeta/lambda.' findings: [] - id: PMID:16814735 title: 'siRNA-based gene silencing reveals specialized roles of IRS-1/Akt2 and IRS-2/Akt1 in glucose and lipid metabolism in human skeletal muscle.' findings: [] - id: PMID:17006541 title: 'Regulation of TopBP1 oligomerization by Akt/PKB for cell survival.' findings: [] - id: PMID:17030608 title: 'BRF1 protein turnover and mRNA decay activity are regulated by protein kinase B at the same phosphorylation sites.' findings: [] - id: PMID:17386266 title: 'PRAS40 is an insulin-regulated inhibitor of the mTORC1 protein kinase.' findings: [] - id: PMID:17554339 title: 'Akt/PKB regulates hepatic metabolism by directly inhibiting PGC-1alpha transcription coactivator.' findings: [] - id: PMID:17577629 title: 'Akt/PKB interacts with the histone H3 methyltransferase SETDB1 and coordinates to silence gene expression.' findings: [] - id: PMID:17925406 title: 'Activation of the insulin receptor by insulin and a synthetic peptide leads to divergent metabolic and mitogenic signaling and responses.' findings: [] - id: PMID:17932490 title: 'The pro-apoptotic kinase Mst1 and its caspase cleavage products are direct inhibitors of Akt1.' findings: [] - id: PMID:18191226 title: 'A beta-arrestin 2 signaling complex mediates lithium action on behavior.' findings: [] - id: PMID:18292230 title: 'Akt and CHIP coregulate tau degradation through coordinated interactions.' findings: - statement: AKT1 can prevent CHIP-mediated tau ubiquitination and degradation. supporting_text: Akt also prevents CHIP-induced tau ubiquitination and its subsequent degradation. - id: PMID:18387192 title: 'A pathway sensor for genome-wide screens of intracellular proteolytic cleavage.' findings: - statement: AKT1 knockdown enhanced LC3 reporter release, consistent with AKT1 acting as a negative regulator of autophagy. supporting_text: Knockdown of AKT1 resulted in an increase of dNGLUC release from cells expressing Actin-LC3-dNGLUC. - id: PMID:18456494 title: 'Synthesis and structure based optimization of novel Akt inhibitors.' findings: - statement: X-ray co-crystal structures of pyrrolopyrimidine inhibitors bound to the AKT1 kinase domain (PDB 3CQU, 3CQW; 3CQW also contains Mn) define the kinase active site/ATP pocket and key inhibitor binding interactions, supporting AKT1 protein serine/threonine kinase activity and ATP binding. supporting_text: Akt kinase are explored. X-ray co-crystal structures of two lead series results reference_review: relevance: MEDIUM correctness: VERIFIED review_notes: Medicinal-chemistry structure-based optimization of pyrrolopyrimidine Akt inhibitors whose X-ray co-crystal structures with the AKT1 kinase domain (PDB 3CQU/3CQW) resolve the kinase active site and ATP pocket, confirming the kinase domain/ATP-binding site without characterizing physiological substrate phosphorylation. - id: PMID:18483258 title: 'UVA-induced cell cycle progression is mediated by a disintegrin and metalloprotease/epidermal growth factor receptor/AKT/Cyclin D1 pathways in keratinocytes.' findings: [] - id: PMID:18505846 title: 'p53 stabilization in response to DNA damage requires Akt/PKB and DNA-PK.' findings: [] - id: PMID:18558630 title: 'Overlapping and distinct roles for PI3Kbeta and gamma isoforms in S1P-induced migration of human and mouse endothelial cells.' findings: [] - id: PMID:18562279 title: 'Akt phosphorylation and nuclear phosphoinositide association mediate mRNA export and cell proliferation activities by ALY.' findings: [] - id: PMID:18624398 title: 'Protein interaction data set highlighted with human Ras-MAPK/PI3K signaling pathways.' findings: [] - id: PMID:18650932 title: 'Par-4 inhibits Akt and suppresses Ras-induced lung tumorigenesis.' findings: [] - id: PMID:18786403 title: 'Structural basis for DNA recognition by FoxO1 and its regulation by posttranslational modification.' findings: [] - id: PMID:19057511 title: 'PTEN regulation by Akt-EGR1-ARF-PTEN axis.' findings: [] - id: PMID:19122674 title: 'Deficiency of a beta-arrestin-2 signal complex contributes to insulin resistance.' findings: [] - id: PMID:19126672 title: 'Spontaneous phosphoinositide 3-kinase signaling dynamics drive spreading and random migration of fibroblasts.' findings: [] - id: PMID:19162005 title: 'Response gene to complement 32 is required for C5b-9 induced cell cycle activation in endothelial cells.' findings: [] - id: PMID:19166854 title: '14-3-3 Binding to Pim-phosphorylated Ser166 and Ser186 of human Mdm2--Potential interplay with the PKB/Akt pathway and p14(ARF).' findings: [] - id: PMID:19197339 title: 'Regulation of human myoblast differentiation by PEBP4.' findings: [] - id: PMID:19203586 title: 'PH domain-only protein PHLDA3 is a p53-regulated repressor of Akt.' findings: [] - id: PMID:19262695 title: 'c-Src regulates Akt signaling in response to ghrelin via beta-arrestin signaling-independent and -dependent mechanisms.' findings: [] - id: PMID:19541650 title: 'Signaling mechanisms involved in altered function of macrophages from diet-induced obese mice affect immune responses.' findings: [] - id: PMID:19573808 title: 'EphA2 mediates ligand-dependent inhibition and ligand-independent promotion of cell migration and invasion via a reciprocal regulatory loop with Akt.' findings: [] - id: PMID:19667065 title: 'Identification of novel in vivo phosphorylation sites of the human proapoptotic protein BAD: pore-forming activity of BAD is regulated by phosphorylation.' findings: [] - id: PMID:19698782 title: 'Evidence for the involvement of FAM110C protein in cell spreading and migration.' findings: [] - id: PMID:19713527 title: 'The E3 ligase TRAF6 regulates Akt ubiquitination and activation.' findings: [] - id: PMID:19850054 title: 'Semaphorin 5A promotes angiogenesis by increasing endothelial cell proliferation, migration, and decreasing apoptosis.' findings: [] - id: PMID:19903888 title: 'DAB2IP coordinates both PI3K-Akt and ASK1 pathways for cell survival and apoptosis.' findings: [] - id: PMID:19934221 title: 'The Rho-family GEF Asef2 activates Rac to modulate adhesion and actin dynamics and thereby regulate cell migration.' findings: [] - id: PMID:20011604 title: 'A phosphoinositide 3-kinase/phospholipase Cgamma1 pathway regulates fibroblast growth factor-induced capillary tube formation.' findings: [] - id: PMID:20059950 title: 'The E3 ligase TTC3 facilitates ubiquitination and degradation of phosphorylated Akt.' findings: [] - id: PMID:20086174 title: 'Proapoptotic kinase MST2 coordinates signaling crosstalk between RASSF1A, Raf-1, and Akt.' findings: [] - id: PMID:20186153 title: 'Protein phosphatase-1 regulates Akt1 signal transduction pathway to control gene expression, cell survival and differentiation.' findings: [] - id: PMID:20237237 title: 'COMMD1 downregulates the epithelial sodium channel through Nedd4-2.' findings: [] - id: PMID:20333297 title: 'Ack1 mediated AKT/PKB tyrosine 176 phosphorylation regulates its activation.' findings: [] - id: PMID:20605787 title: 'Ribosomal protein S3, a new substrate of Akt, serves as a signal mediator between neuronal apoptosis and DNA repair.' findings: [] - id: PMID:20650008 title: 'Degradation of HER2/neu by ANT2 shRNA suppresses migration and invasiveness of breast cancer cells.' findings: [] - id: PMID:20682768 title: 'Phosphorylation of CLK2 at serine 34 and threonine 127 by AKT controls cell survival after ionizing radiation.' findings: [] - id: PMID:20856200 title: 'Vimentin is a novel AKT1 target mediating motility and invasion.' findings: [] - id: PMID:20878056 title: 'Critical involvement of RQCD1 in the EGFR-Akt pathway in mammary carcinogenesis.' findings: [] - id: PMID:21044950 title: 'Genome-wide YFP fluorescence complementation screen identifies new regulators for telomere signaling in human cells.' findings: [] - id: PMID:21045808 title: 'mTORC2 can associate with ribosomes to promote cotranslational phosphorylation and stability of nascent Akt polypeptide.' findings: [] - id: PMID:21151116 title: 'A methylation and phosphorylation switch between an adjacent lysine and serine determines human DNMT1 stability.' findings: [] - id: PMID:21177249 title: 'A new cytosolic pathway from a Parkinson disease-associated kinase, BRPK/PINK1: activation of AKT via mTORC2.' findings: [] - id: PMID:21321938 title: 'Interleukin-18/WNT1-inducible signaling pathway protein-1 signaling mediates human saphenous vein smooth muscle cell proliferation.' findings: [] - id: PMID:21333377 title: 'Ret finger protein 2 enhances ionizing radiation-induced apoptosis via degradation of AKT and MDM2.' findings: [] - id: PMID:21432781 title: 'Akt1 and Akt2: differentiating the aktion.' findings: [] - id: PMID:21621563 title: 'Bimodal regulation of FoxO3 by AKT and 14-3-3.' findings: [] - id: PMID:21658387 title: 'LRRK2 directly phosphorylates Akt1 as a possible physiological substrate: impairment of the kinase activity by Parkinson''s disease-associated mutations.' findings: [] - id: PMID:21711983 title: 'A role for Akt and glycogen synthase kinase-3 as integrators of dopamine and serotonin neurotransmission in mental health.' findings: [] - id: PMID:21775285 title: 'The deacetylase SIRT1 promotes membrane localization and activation of Akt and PDK1 during tumorigenesis and cardiac hypertrophy.' findings: [] - id: PMID:22309289 title: 'Akt augments the oncogenic potential of the HBx protein of hepatitis B virus by phosphorylation.' findings: [] - id: PMID:22510990 title: 'AKT-dependent phosphorylation of Niban regulates nucleophosmin- and MDM2-mediated p53 stability and cell apoptosis.' findings: [] - id: PMID:22797923 title: 'ZNRF2 is released from membranes by growth factors and, together with ZNRF1, regulates the Na+/K+ATPase.' findings: [] - id: PMID:22869525 title: 'Insulin-like growth factor (IGF) binding protein 2 functions coordinately with receptor protein tyrosine phosphatase β and the IGF-I receptor to regulate IGF-I-stimulated signaling.' findings: [] - id: PMID:23010592 title: 'NOK/STYK1 interacts with GSK-3β and mediates Ser9 phosphorylation through activated Akt.' findings: [] - id: PMID:23223530 title: 'Protein kinase N1, a cell inhibitor of Akt kinase, has a central role in quality control of germinal center formation.' findings: [] - id: PMID:23251525 title: 'Microarray-assisted pathway analysis identifies MT1X & NFκB as mediators of TCRP1-associated resistance to cisplatin in oral squamous cell carcinoma.' findings: [] - id: PMID:23300339 title: 'BSTA promotes mTORC2-mediated phosphorylation of Akt1 to suppress expression of FoxC2 and stimulate adipocyte differentiation.' findings: [] - id: PMID:23397142 title: 'Analysis of protein-protein interactions in cross-talk pathways reveals CRKL protein as a novel prognostic marker in hepatocellular carcinoma.' findings: [] - id: PMID:23431171 title: 'MOZ increases p53 acetylation and premature senescence through its complex formation with PML.' findings: [] - id: PMID:23434580 title: 'Akt kinase targets the association of CBP with histone H3 to regulate the acetylation of lysine K18.' findings: [] - id: PMID:23512198 title: 'SCF E3 ligase F-box protein complex SCF(FBXL19) regulates cell migration by mediating Rac1 ubiquitination and degradation.' findings: - statement: AKT-mediated Rac1 phosphorylation supports FBXL19-mediated Rac1 ubiquitination and degradation. supporting_text: Protein kinase AKT-mediated phosphorylation of Rac1 at serine(71) was essential for FBXL19-mediated Rac1 ubiquitination. - id: PMID:23676467 title: 'FAM83B-mediated activation of PI3K/AKT and MAPK signaling cooperates to promote epithelial cell transformation and resistance to targeted therapies.' findings: [] - id: PMID:23693014 title: 'Activation of Akt pathway by transcription-independent mechanisms of retinoic acid promotes survival and invasion in lung cancer cells.' findings: [] - id: PMID:23778976 title: 'IκB kinase complex (IKK) triggers detachment-induced autophagy in mammary epithelial cells independently of the PI3K-AKT-MTORC1 pathway.' findings: - statement: PI3K-AKT-MTORC1 effects on autophagy are context dependent in detachment-induced autophagy models. supporting_text: Enforced activation of this pathway is not sufficient to suppress detachment-induced autophagy in MECs. - id: PMID:23962723 title: 'Hexokinase activity is required for recruitment of parkin to depolarized mitochondria.' findings: [] - id: PMID:24291004 title: 'Direct reversal of glucocorticoid resistance by AKT inhibition in acute lymphoblastic leukemia.' findings: [] - id: PMID:24412244 title: 'Charting the molecular links between driver and susceptibility genes in colorectal cancer.' findings: [] - id: PMID:24529379 title: 'Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome.' findings: [] - id: PMID:24658140 title: 'The mammalian-membrane two-hybrid assay (MaMTH) for probing membrane-protein interactions in human cells.' findings: [] - id: PMID:24670654 title: 'Cell-cycle-regulated activation of Akt kinase by phosphorylation at its carboxyl terminus.' findings: [] - id: PMID:24784001 title: 'KIF14 promotes AKT phosphorylation and contributes to chemoresistance in triple-negative breast cancer.' findings: [] - id: PMID:25190803 title: 'Unspliced X-box-binding protein 1 (XBP1) protects endothelial cells from oxidative stress through interaction with histone deacetylase 3.' findings: [] - id: PMID:25241761 title: 'Using an in situ proximity ligation assay to systematically profile endogenous protein-protein interactions in a pathway network.' findings: [] - id: PMID:25910212 title: 'Widespread macromolecular interaction perturbations in human genetic disorders.' findings: [] - id: PMID:26118642 title: 'Lysosomal mTORC2/PHLPP1/Akt Regulate Chaperone-Mediated Autophagy.' findings: - statement: Lysosomal Akt1 negatively regulates chaperone-mediated autophagy. supporting_text: Overall, these results support an inhibitory effect of Akt1 on CMA. - statement: AKT1 regulates LAMP-2A translocation-complex dynamics through lysosomal GFAP phosphorylation. supporting_text: Inhibition of Akt activity in isolated lysosomes lead to a similar dose-dependent increase in the amount of CMA translocation complex. - id: PMID:26256536 title: 'The Mechanism of ATP-Dependent Allosteric Protection of Akt Kinase Phosphorylation.' findings: [] - id: PMID:26440888 title: 'Akt Kinase-Mediated Checkpoint of cGAS DNA Sensing Pathway.' findings: [] - id: PMID:26871637 title: 'Widespread Expansion of Protein Interaction Capabilities by Alternative Splicing.' findings: [] - id: PMID:28147277 title: 'Regulation of Serine-Threonine Kinase Akt Activation by NAD(+)-Dependent Deacetylase SIRT7.' findings: [] - id: PMID:28341552 title: 'Identification of a molecular signaling gene-gene regulatory network between GWAS susceptibility genes ADTRP and MIA3/TANGO1 for coronary artery disease.' findings: [] - id: PMID:28386764 title: 'Roles of tau protein in health and disease.' findings: [] - id: PMID:28514442 title: 'Architecture of the human interactome defines protein communities and disease networks.' findings: [] - id: PMID:29104511 title: 'ATP2B1 gene Silencing Increases Insulin Sensitivity through Facilitating Akt Activation via the Ca(2+)/calmodulin Signaling Pathway and Ca(2+)-associated eNOS Activation in Endothelial Cells.' findings: [] - id: PMID:29343641 title: 'Degradation of FBXO31 by APC/C is regulated by AKT- and ATM-mediated phosphorylation.' findings: [] - id: PMID:29997244 title: 'LuTHy: a double-readout bioluminescence-based two-hybrid technology for quantitative mapping of protein-protein interactions in mammalian cells.' findings: [] - id: PMID:30504268 title: 'Akt-mediated phosphorylation of MICU1 regulates mitochondrial Ca(2+) levels and tumor growth.' findings: [] - id: PMID:30514904 title: 'Ubiquitination of Rheb governs growth factor-induced mTORC1 activation.' findings: [] - id: PMID:31204173 title: 'Akt Regulates a Rab11-Effector Switch Required for Ciliogenesis.' findings: [] - id: PMID:31515488 title: 'Extensive disruption of protein interactions by genetic variants across the allele frequency spectrum in human populations.' findings: [] - id: PMID:31548394 title: 'Phosphorylation of DEPDC5, a component of the GATOR1 complex, releases inhibition of mTORC1 and promotes tumor growth.' findings: [] - id: PMID:31915252 title: 'The GATOR2-mTORC2 axis mediates Sestrin2-induced AKT Ser/Thr kinase activation.' findings: [] - id: PMID:31980649 title: 'Extensive rewiring of the EGFR network in colorectal cancer cells expressing transforming levels of KRAS(G13D).' findings: [] - id: PMID:32296183 title: 'A reference map of the human binary protein interactome.' findings: [] - id: PMID:32322062 title: 'The gluconeogenic enzyme PCK1 phosphorylates INSIG1/2 for lipogenesis.' findings: [] - id: PMID:32814053 title: 'Interactome Mapping Provides a Network of Neurodegenerative Disease Proteins and Uncovers Widespread Protein Aggregation in Affected Brains.' findings: [] - id: PMID:33505021 title: 'A growth-factor-activated lysosomal K(+) channel regulates Parkinson''s pathology.' findings: [] - id: PMID:33594058 title: 'RNF167 activates mTORC1 and promotes tumorigenesis by targeting CASTOR1 for ubiquitination and degradation.' findings: [] - id: PMID:33961781 title: 'Dual proteome-scale networks reveal cell-specific remodeling of the human interactome.' findings: [] - id: PMID:34591612 title: 'A protein interaction landscape of breast cancer.' findings: [] - id: PMID:35271311 title: 'OpenCell: Endogenous tagging for the cartography of human cellular organization.' findings: [] - id: PMID:35512704 title: 'Systematic discovery of mutation-directed neo-protein-protein interactions in cancer.' findings: [] - id: PMID:36126419 title: 'MPST deficiency promotes intestinal epithelial cell apoptosis and aggravates inflammatory bowel disease via AKT.' findings: [] - id: PMID:38020884 title: 'Protein kinase B/AKT phosphorylates hypoxia-inducible factor-3α1 in response to insulin, promoting cell growth and migration.' findings: [] - id: PMID:40285646 title: 'm(6)A-Mediated TMCO3 Promotes Hepatocellular Carcinoma Progression by Facilitating the Membrane Translocation and Activation of AKT.' findings: [] - id: PMID:7891724 title: 'AH/PH domain-mediated interaction between Akt molecules and its potential role in Akt regulation.' findings: [] - id: PMID:8524413 title: 'Inhibition of glycogen synthase kinase-3 by insulin mediated by protein kinase B.' findings: [] - id: PMID:8940145 title: 'Expression of a constitutively active Akt Ser/Thr kinase in 3T3-L1 adipocytes stimulates glucose uptake and glucose transporter 4 translocation.' findings: [] - id: PMID:8978681 title: 'Mechanism of activation of protein kinase B by insulin and IGF-1.' findings: [] - id: PMID:9373175 title: 'Further evidence that the inhibition of glycogen synthase kinase-3beta by IGF-1 is mediated by PDK1/PKB-induced phosphorylation of Ser-9 and not by dephosphorylation of Tyr-216.' findings: [] - id: Reactome:R-HSA-1358791 title: 'Phosphorylation of USP8 by P-AKT' findings: [] - id: Reactome:R-HSA-1497784 title: 'The cofactor BH4 is required for electron transfer in the eNOS catalytic cycle' findings: [] - id: Reactome:R-HSA-1497796 title: 'BH2 binding can lead to eNOS uncoupling' findings: [] - id: Reactome:R-HSA-1497810 title: 'Uncoupled eNOS favours the formation of superoxide' findings: [] - id: Reactome:R-HSA-198270 title: 'PDPK1 phosphorylates AKT at T308' findings: [] - id: Reactome:R-HSA-198599 title: 'AKT phosphorylates MDM2' findings: [] - id: Reactome:R-HSA-198609 title: 'AKT phosphorylates TSC2, inhibiting it' findings: [] - id: Reactome:R-HSA-198611 title: 'AKT phosphorylates IKKalpha' findings: [] - id: Reactome:R-HSA-198613 title: 'AKT phosphorylates p21Cip1 and p27Kip1' findings: [] - id: Reactome:R-HSA-198621 title: 'AKT phosphorylates caspase-9' findings: [] - id: Reactome:R-HSA-198640 title: 'mTORC2 phosphorylates AKT at S473' findings: [] - id: Reactome:R-HSA-199298 title: 'AKT phosphorylates CREB1' findings: [] - id: Reactome:R-HSA-199299 title: 'AKT phosphorylates FOXO transcription factors' findings: [] - id: Reactome:R-HSA-199425 title: 'PHLPP dephosphorylates S473 in AKT' findings: [] - id: Reactome:R-HSA-199443 title: 'THEM4 (CTMP) and/or TRIB3 inhibit AKT phosphorylation' findings: [] - id: Reactome:R-HSA-199839 title: 'AKT can phosphorylate RSK' findings: [] - id: Reactome:R-HSA-199863 title: 'AKT can phosphorylate NR4A1 (NUR77)' findings: [] - id: Reactome:R-HSA-200143 title: 'AKT phosphorylates AKT1S1 (PRAS40)' findings: [] - id: Reactome:R-HSA-202111 title: 'AKT1 phosphorylates eNOS' findings: [] - id: Reactome:R-HSA-202127 title: 'eNOS synthesizes NO' findings: [] - id: Reactome:R-HSA-202137 title: 'AKT1 binds eNOS complex via HSP90' findings: [] - id: Reactome:R-HSA-203615 title: 'eNOS activation' findings: [] - id: Reactome:R-HSA-211163 title: 'AKT-mediated inactivation of FOXO1A' findings: [] - id: Reactome:R-HSA-211164 title: 'AKT phosphorylates FOXO1A' findings: [] - id: Reactome:R-HSA-2219536 title: 'AKT1 E17K mutant binds PIP2' findings: [] - id: Reactome:R-HSA-2243937 title: 'PIP2-bound p-S473-AKT1 mutant binds PIP2-bound PDPK1' findings: [] - id: Reactome:R-HSA-2243938 title: 'AKT1 E17K mutant is phosphorylated by TORC2 complex' findings: [] - id: Reactome:R-HSA-2243942 title: 'PDPK1 phosphorylates AKT1 E17K mutant' findings: [] - id: Reactome:R-HSA-2262752 title: 'Cellular responses to stress' findings: [] - id: Reactome:R-HSA-2317314 title: 'AKT binds PDPK1' findings: [] - id: Reactome:R-HSA-2317332 title: 'PIP3 recruits AKT to the membrane' findings: [] - id: Reactome:R-HSA-2399941 title: 'AKT1 E17K mutant phosphorylates BAD' findings: [] - id: Reactome:R-HSA-2399966 title: 'AKT1 E17K mutant phosphorylates GSK3' findings: [] - id: Reactome:R-HSA-2399969 title: 'AKT1 E17K mutant phosphorylates p21Cip1 and p27Kip1' findings: [] - id: Reactome:R-HSA-2399977 title: 'AKT1 E17K mutant phosphorylates AKT1S1 (PRAS40)' findings: [] - id: Reactome:R-HSA-2399981 title: 'AKT1 E17K mutant phosphorylates MDM2' findings: [] - id: Reactome:R-HSA-2399982 title: 'AKT1 E17K mutant phosphorylates TSC2, inhibiting it' findings: [] - id: Reactome:R-HSA-2399985 title: 'AKT1 E17K mutant phosphorylates caspase-9' findings: [] - id: Reactome:R-HSA-2399988 title: 'AKT1 E17K mutant phosphorylates NR4A1 (NUR77)' findings: [] - id: Reactome:R-HSA-2399992 title: 'AKT1 E17K mutant phosphorylates forkhead box transcription factors' findings: [] - id: Reactome:R-HSA-2399996 title: 'AKT1 E17K mutant phosphorylates CREB1' findings: [] - id: Reactome:R-HSA-2399997 title: 'AKT1 E17K mutant translocates to the nucleus' findings: [] - id: Reactome:R-HSA-2399999 title: 'AKT1 E17K mutant phosphorylates RSK' findings: [] - id: Reactome:R-HSA-2400001 title: 'AKT1 E17K mutant phosphorylates CHUK (IKKalpha)' findings: [] - id: Reactome:R-HSA-2400010 title: 'AKT inhibitors block AKT membrane recruitment' findings: [] - id: Reactome:R-HSA-3769394 title: 'AKT phosphorylates CBY1' findings: [] - id: Reactome:R-HSA-377186 title: 'Activated AKT phosphorylates AKT1S1 (PRAS40)' findings: [] - id: Reactome:R-HSA-389356 title: 'Co-stimulation by CD28' findings: [] - id: Reactome:R-HSA-389756 title: 'AKT interacts and phosphorylates Cot' findings: [] - id: Reactome:R-HSA-390329 title: 'Dephosphorylation of AKT by PP2A' findings: [] - id: Reactome:R-HSA-432110 title: 'Integrin alpha IIb beta3 T779 phosphorylation blocks SHC binding' findings: [] - id: Reactome:R-HSA-450385 title: 'Butyrate Response Factor 1 (BRF1) binds and destabilizes mRNA' findings: [] - id: Reactome:R-HSA-450490 title: 'Protein Kinase B/Akt phosphorylates BRF1' findings: [] - id: Reactome:R-HSA-450499 title: 'Protein Kinase B (AKT) phosphorylates KSRP' findings: [] - id: Reactome:R-HSA-450604 title: 'KSRP (KHSRP) binds and destabilizes mRNA' findings: [] - id: Reactome:R-HSA-6790041 title: 'Expression of STAT3-upregulated cytosolic proteins' findings: [] - id: Reactome:R-HSA-6804758 title: 'Regulation of TP53 Activity through Acetylation' findings: [] - id: Reactome:R-HSA-6804759 title: 'Regulation of TP53 Activity through Association with Co-factors' findings: [] - id: Reactome:R-HSA-6805640 title: 'AKT phosphorylates KAT6A' findings: [] - id: Reactome:R-HSA-6805785 title: 'AKT phosphorylates PHF20' findings: [] - id: Reactome:R-HSA-6811504 title: 'AKT1 dephosphorylation by PP2A-B56-beta,gamma' findings: [] - id: Reactome:R-HSA-8848751 title: 'PTK6 binds AKT1' findings: [] - id: Reactome:R-HSA-8848758 title: 'PTK6 phosphorylates AKT1' findings: [] - id: Reactome:R-HSA-8933446 title: 'Active AKT phosphorylates DENND1A and DENND1B in response to insulin signaling' findings: [] - id: Reactome:R-HSA-8948757 title: 'AKT phosphorylates MKRN1' findings: [] - id: Reactome:R-HSA-9603279 title: 'PIP3 recruits PDK1 and AKT to the membrane' findings: [] - id: Reactome:R-HSA-9604328 title: 'AKT1 phosphorylates NOTCH4' findings: [] - id: Reactome:R-HSA-9607240 title: 'FLT3 Signaling' findings: [] - id: Reactome:R-HSA-9624526 title: 'AKT phosphorylates FOXO3 downstream of ESR1 and EGFR' findings: [] - id: Reactome:R-HSA-9699579 title: 'AKT phosphorylates FOXO3 downstream of FLT3 ' findings: [] - id: Reactome:R-HSA-9841244 title: 'Phosphorylation of AKT1 on serine-473 in response to reactive oxygen species' findings: [] - id: Reactome:R-HSA-9841265 title: 'p-S473-AKT1 phosphorylates ESR1 on serine-167' findings: [] - id: Reactome:R-HSA-9856530 title: 'High laminar flow shear stress activates signaling by PIEZO1 and PECAM1:CDH5:KDR in endothelial cells' findings: [] - id: Reactome:R-HSA-9860759 title: 'p-T816-PKN2 phosphorylates AKT1 on serine-308' findings: [] - id: Reactome:R-HSA-9860792 title: 'Phospho-AKT1 phosphorylates NOS3 (eNOS) on serine-1177' findings: [] - id: Reactome:R-HSA-9860800 title: 'mTORC2 phosphorylates AKT1 on serine-473' findings: [] - id: Reactome:R-NUL-3139045 title: 'AKT phosphorylates Bad' findings: [] - id: Reactome:R-NUL-8939977 title: 'Activated AKT1 phosphorylates Runx2' findings: [] - id: file:human/AKT1/AKT1-uniprot.txt title: UniProt text export for AKT1 findings: - statement: UniProt identifies AKT1 and its protein family/domain context. supporting_text: Belongs to the protein kinase superfamily. AGC Ser/Thr - id: file:human/AKT1/AKT1-deep-research-falcon.md title: Falcon deep research report for AKT1 findings: - statement: Falcon research supports the reviewed core function of AKT1. supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - id: file:projects/PROTEOSTASIS/reports/pn_projection/pn_projected_gene_go_summary.tsv title: Proteostasis PN projected gene GO summary findings: - statement: The PN projection maps AKT1 to negative regulation of chaperone-mediated autophagy as a more specific term than existing GOA. supporting_text: AKT1 GO:1904715 negative regulation of chaperone-mediated autophagy more_specific_than_existing_goa. - id: file:projects/PROTEOSTASIS/mappings/autophagy_lysosome_pathway.yaml title: Proteostasis PN autophagy-lysosome pathway mappings findings: - statement: The PN CMA inhibitor type maps to negative regulation of chaperone-mediated autophagy, while the LAMP2A multimerization subtype is contextual. supporting_text: This PN type explicitly records inhibitory roles for CMA. core_functions: - description: PI3K-regulated protein serine/threonine kinase activity that phosphorylates substrates controlling growth, metabolism, survival, and mTOR-linked signaling. molecular_function: id: GO:0004674 label: protein serine/threonine kinase activity directly_involved_in: - id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction - id: GO:0006468 label: protein phosphorylation locations: - id: GO:0005829 label: cytosol - id: GO:0005886 label: plasma membrane - id: GO:0005634 label: nucleus supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. - description: PH-domain lipid binding that recruits AKT1 to phosphoinositide-rich membranes for activation by PDK1 and mTORC2. molecular_function: id: GO:0005547 label: phosphatidylinositol-3,4,5-trisphosphate binding directly_involved_in: - id: GO:0043491 label: phosphatidylinositol 3-kinase/protein kinase B signal transduction locations: - id: GO:0005886 label: plasma membrane supported_by: - reference_id: file:human/AKT1/AKT1-deep-research-falcon.md supporting_text: AKT1 is a **serine/threonine protein kinase** (PKB) that is activated downstream of receptor tyrosine kinases (RTKs), GPCRs, and insulin receptor substrates (IRS) via PI3K lipid signaling. proposed_new_terms: [] suggested_questions: - question: Which AKT1 substrate phosphorylation events should be represented as direct GO annotations rather than downstream pathway outcomes? - question: How should AKT1-specific functions be separated from overlapping AKT2 and AKT3 biology in human pathway annotations? - question: Should AKT1 negative regulation of chaperone-mediated autophagy be curated broadly for AKT1, or limited to lysosomal TORC2/PHLPP1/Akt evidence contexts? suggested_experiments: - description: Quantitative phosphoproteomics after endogenous AKT1 inhibition or degron-mediated depletion with AKT2/AKT3 controls. experiment_type: phosphoproteomics/genome editing hypothesis: Direct AKT1 substrates can be separated from broad downstream pathway responses. - description: Live-cell imaging of endogenous AKT1 membrane recruitment with PH-domain mutants and pathway activation markers. experiment_type: live-cell imaging/signaling assay hypothesis: PIP3 binding and membrane recruitment define the core activation step for AKT1 kinase signaling.