Hras encodes the membrane-anchored Ras-family small GTPase H-Ras, a GDP/GTP molecular switch that relays receptor-derived signals to RAF-MEK-ERK, PI3K, RalGEF, and related effector pathways. Core function is GTP binding/hydrolysis and GTP-state-dependent effector recruitment at plasma-membrane and Golgi/endomembrane compartments after CAAX processing and reversible palmitoylation. Proliferation, senescence, differentiation, neural, immune, and wound-response phenotypes are curated as downstream or specialized contexts unless the annotation directly describes Ras switch activity or membrane-localized Ras signal transduction.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005886 plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0007265 Ras protein signal transduction | IBA GO_REF:0000033 | ACCEPT | Summary: Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0008284 positive regulation of cell population proliferation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0003924 GTPase activity | IBA GO_REF:0000033 | ACCEPT | Summary: GTPase activity is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0090398 cellular senescence | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: cellular senescence is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0000139 Golgi membrane | IEA GO_REF:0000044 | ACCEPT | Summary: Golgi membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0003924 GTPase activity | IEA GO_REF:0000120 | ACCEPT | Summary: GTPase activity is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0003925 G protein activity | IEA GO_REF:0000003 | ACCEPT | Summary: G protein activity is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0005525 GTP binding | IEA GO_REF:0000120 | ACCEPT | Summary: GTP binding is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005794 Golgi apparatus | IEA GO_REF:0000120 | ACCEPT | Summary: Golgi apparatus is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005886 plasma membrane | IEA GO_REF:0000120 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0007165 signal transduction | IEA GO_REF:0000002 | MODIFY | Summary: Signal transduction is too broad for H-Ras. Reason: H-Ras is specifically a Ras-family small GTPase in Ras protein signal transduction. Proposed replacements: Ras protein signal transduction Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0016020 membrane | IEA GO_REF:0000002 | MODIFY | Summary: Membrane is too broad for H-Ras localization. Reason: H-Ras signaling depends on processed and palmitoylated localization at plasma membrane and Golgi/endomembrane compartments. Proposed replacements: plasma membrane Golgi membrane Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005515 protein binding | IPI PMID:9488663 Identification of Nore1 as a potential Ras effector. | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005654 nucleoplasm | IEA GO_REF:0000120 | UNDECIDED | Summary: The current local evidence does not provide term-specific support for H-Ras localization to the nucleoplasm. Reason: Automated localization transfer requires direct compartment evidence before retaining this annotation. |
| GO:0005829 cytosol | IEA GO_REF:0000120 | ACCEPT | Summary: cytosol is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-uniprot.txt DR GO; GO:0005829; C:cytosol; ISO:GO_Central. file:mouse/Hras/Hras-deep-research-falcon.md Nascent Ras proteins undergo processing in cytosol/ER and further modifications enabling targeting to the **inner leaflet of the plasma membrane** |
| GO:0006357 regulation of transcription by RNA polymerase II | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: regulation of transcription by RNA polymerase II is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0007265 Ras protein signal transduction | IEA GO_REF:0000107 | ACCEPT | Summary: Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0008284 positive regulation of cell population proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0008285 negative regulation of cell population proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0010629 negative regulation of gene expression | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of gene expression is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0019003 GDP binding | IEA GO_REF:0000107 | ACCEPT | Summary: GDP binding is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0030335 positive regulation of cell migration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of cell migration is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0032956 regulation of actin cytoskeleton organization | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: regulation of actin cytoskeleton organization is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0042127 regulation of cell population proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0043410 positive regulation of MAPK cascade | IEA GO_REF:0000107 | ACCEPT | Summary: positive regulation of MAPK cascade is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of transcription by RNA polymerase II is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0046330 positive regulation of JNK cascade | IEA GO_REF:0000107 | ACCEPT | Summary: positive regulation of JNK cascade is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0050679 positive regulation of epithelial cell proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of epithelial cell proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0070374 positive regulation of ERK1 and ERK2 cascade | IEA GO_REF:0000107 | ACCEPT | Summary: positive regulation of ERK1 and ERK2 cascade is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0071480 cellular response to gamma radiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to gamma radiation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090303 positive regulation of wound healing | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of wound healing is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090314 positive regulation of protein targeting to membrane | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of protein targeting to membrane is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090398 cellular senescence | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular senescence is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0098696 regulation of neurotransmitter receptor localization to postsynaptic specialization membrane | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: regulation of neurotransmitter receptor localization to postsynaptic specialization membrane is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0098978 glutamatergic synapse | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: glutamatergic synapse is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0160185 phospholipase C activator activity | IEA GO_REF:0000107 | UNDECIDED | Summary: The current local evidence supports RAF, PI3K, and RalGEF effector signaling, but does not establish phospholipase C activator activity for H-Ras. Reason: Retaining this specific molecular function requires direct PLC activation evidence. |
| GO:1900029 positive regulation of ruffle assembly | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of ruffle assembly is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:2000630 positive regulation of miRNA metabolic process | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of miRNA metabolic process is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0005794 Golgi apparatus | ISO GO_REF:0000119 | ACCEPT | Summary: Golgi apparatus is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005886 plasma membrane | ISO GO_REF:0000119 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0000164 protein phosphatase type 1 complex | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: The PP1 complex term does not describe the H-Ras core function. Reason: H-Ras may influence or associate with regulatory complexes in particular studies, but the core function is membrane-localized GDP/GTP switch signaling. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0003924 GTPase activity | ISO GO_REF:0000119 | ACCEPT | Summary: GTPase activity is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0005525 GTP binding | ISO GO_REF:0000119 | ACCEPT | Summary: GTP binding is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005654 nucleoplasm | ISO GO_REF:0000119 | UNDECIDED | Summary: The current local evidence does not provide term-specific support for H-Ras localization to the nucleoplasm. Reason: Automated localization transfer requires direct compartment evidence before retaining this annotation. |
| GO:0005829 cytosol | ISO GO_REF:0000119 | ACCEPT | Summary: cytosol is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-uniprot.txt DR GO; GO:0005829; C:cytosol; ISO:GO_Central. file:mouse/Hras/Hras-deep-research-falcon.md Nascent Ras proteins undergo processing in cytosol/ER and further modifications enabling targeting to the **inner leaflet of the plasma membrane** |
| GO:0005886 plasma membrane | ISO GO_REF:0000096 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0006357 regulation of transcription by RNA polymerase II | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: regulation of transcription by RNA polymerase II is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0007265 Ras protein signal transduction | ISO GO_REF:0000119 | ACCEPT | Summary: Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0008284 positive regulation of cell population proliferation | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0008285 negative regulation of cell population proliferation | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: negative regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0010629 negative regulation of gene expression | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: negative regulation of gene expression is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0019003 GDP binding | ISO GO_REF:0000119 | ACCEPT | Summary: GDP binding is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0030335 positive regulation of cell migration | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of cell migration is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0032956 regulation of actin cytoskeleton organization | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: regulation of actin cytoskeleton organization is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0036064 ciliary basal body | ISO GO_REF:0000119 | UNDECIDED | Summary: The current local evidence does not provide term-specific support for H-Ras localization to the ciliary basal body. Reason: Automated localization transfer requires direct compartment evidence before retaining this annotation. |
| GO:0042127 regulation of cell population proliferation | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0043410 positive regulation of MAPK cascade | ISO GO_REF:0000119 | ACCEPT | Summary: positive regulation of MAPK cascade is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0044877 protein-containing complex binding | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: protein-containing complex binding is too generic to represent the core H-Ras molecular function; the informative biology is GTPase switch activity and effector-pathway activation. Reason: Use GTPase/GTP binding and Ras pathway terms rather than retaining a broad binding term as core. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0045944 positive regulation of transcription by RNA polymerase II | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of transcription by RNA polymerase II is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0046330 positive regulation of JNK cascade | ISO GO_REF:0000119 | ACCEPT | Summary: positive regulation of JNK cascade is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0050679 positive regulation of epithelial cell proliferation | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of epithelial cell proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0051726 regulation of cell cycle | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: regulation of cell cycle is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0070374 positive regulation of ERK1 and ERK2 cascade | ISO GO_REF:0000119 | ACCEPT | Summary: positive regulation of ERK1 and ERK2 cascade is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0071480 cellular response to gamma radiation | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: cellular response to gamma radiation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090303 positive regulation of wound healing | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of wound healing is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090314 positive regulation of protein targeting to membrane | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of protein targeting to membrane is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090398 cellular senescence | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: cellular senescence is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0098696 regulation of neurotransmitter receptor localization to postsynaptic specialization membrane | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: regulation of neurotransmitter receptor localization to postsynaptic specialization membrane is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0098978 glutamatergic synapse | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: glutamatergic synapse is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0160185 phospholipase C activator activity | ISO GO_REF:0000119 | UNDECIDED | Summary: The current local evidence supports RAF, PI3K, and RalGEF effector signaling, but does not establish phospholipase C activator activity for H-Ras. Reason: Retaining this specific molecular function requires direct PLC activation evidence. |
| GO:1900029 positive regulation of ruffle assembly | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of ruffle assembly is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:1905360 GTPase complex | ISO GO_REF:0000119 | ACCEPT | Summary: GTPase complex is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:2000630 positive regulation of miRNA metabolic process | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of miRNA metabolic process is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0005886 plasma membrane | ISO PMID:19878719 RGS14 is a multifunctional scaffold that integrates G protei... | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0090402 oncogene-induced cell senescence | IDA PMID:11551927 The ink4a/arf tumor suppressors cooperate with p21cip1/waf i... | KEEP AS NON CORE | Summary: oncogene-induced cell senescence is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0043495 protein-membrane adaptor activity | IDA PMID:16405865 Merlin inhibits growth hormone-regulated Raf-ERKs pathways b... | KEEP AS NON CORE | Summary: protein-membrane adaptor activity is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0048009 insulin-like growth factor receptor signaling pathway | ISO PMID:8828504 Comparison of the insulin and insulin-like growth factor 1 m... | KEEP AS NON CORE | Summary: insulin-like growth factor receptor signaling pathway is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0008286 insulin receptor signaling pathway | IDA PMID:7829473 Disassembly of Son-of-sevenless proteins from Grb2 during p2... | KEEP AS NON CORE | Summary: insulin receptor signaling pathway is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090398 cellular senescence | IDA PMID:12878730 The p53-dependent effects of macrophage migration inhibitory... | KEEP AS NON CORE | Summary: cellular senescence is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0090398 cellular senescence | IDA PMID:15572682 Functional genetic screen for genes involved in senescence: ... | KEEP AS NON CORE | Summary: cellular senescence is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0014044 Schwann cell development | IMP PMID:10704452 A dual role of erbB2 in myelination and in expansion of the ... | KEEP AS NON CORE | Summary: Schwann cell development is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0042552 myelination | IMP PMID:10704452 A dual role of erbB2 in myelination and in expansion of the ... | KEEP AS NON CORE | Summary: myelination is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0042552 myelination | IMP PMID:18760695 Neuregulin-1/ErbB signaling serves distinct functions in mye... | KEEP AS NON CORE | Summary: myelination is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0007265 Ras protein signal transduction | ISO PMID:33331896 Merlin cooperates with neurofibromin and Spred1 to suppress ... | ACCEPT | Summary: Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0038133 ERBB2-ERBB3 signaling pathway | ISO PMID:11173924 Neuregulin-induced association of Sos Ras exchange protein w... | KEEP AS NON CORE | Summary: ERBB2-ERBB3 signaling pathway is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0043495 protein-membrane adaptor activity | ISO PMID:33331896 Merlin cooperates with neurofibromin and Spred1 to suppress ... | KEEP AS NON CORE | Summary: protein-membrane adaptor activity is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0060612 adipose tissue development | IMP PMID:31408278 Silencing of lncRNA SNHG20 delays the progression of nonalco... | KEEP AS NON CORE | Summary: adipose tissue development is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0048169 regulation of long-term neuronal synaptic plasticity | IMP PMID:12427827 SynGAP regulates ERK/MAPK signaling, synaptic plasticity, an... | KEEP AS NON CORE | Summary: regulation of long-term neuronal synaptic plasticity is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0005515 protein binding | IPI PMID:16954213 Activation of Ras up-regulates pro-apoptotic BNIP3 in nitric... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0008284 positive regulation of cell population proliferation | IPI PMID:14712229 G-protein-coupled receptor-mediated activation of rap GTPase... | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0007265 Ras protein signal transduction | IGI PMID:11877426 Nerve growth factor-dependent activation of the small GTPase... | ACCEPT | Summary: Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0032729 positive regulation of type II interferon production | IMP PMID:21444916 H-ras and N-ras are dispensable for T-cell development and a... | KEEP AS NON CORE | Summary: positive regulation of type II interferon production is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0042088 T-helper 1 type immune response | IMP PMID:21444916 H-ras and N-ras are dispensable for T-cell development and a... | KEEP AS NON CORE | Summary: T-helper 1 type immune response is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0042832 defense response to protozoan | IMP PMID:21444916 H-ras and N-ras are dispensable for T-cell development and a... | KEEP AS NON CORE | Summary: defense response to protozoan is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0050852 T cell receptor signaling pathway | IMP PMID:21444916 H-ras and N-ras are dispensable for T-cell development and a... | KEEP AS NON CORE | Summary: T cell receptor signaling pathway is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0005515 protein binding | IPI PMID:23382219 Structural basis for endosomal trafficking of diverse transm... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005886 plasma membrane | ISO PMID:17724343 Spatial regulation of Raf kinase signaling by RKTG. | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005515 protein binding | IPI PMID:8939998 RhoGDI-3 is a new GDP dissociation inhibitor (GDI). Identifi... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005515 protein binding | IPI PMID:10869344 A novel RalGEF-like protein, RGL3, as a candidate effector f... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005515 protein binding | IPI PMID:18596699 Novel type of Ras effector interaction established between t... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0097193 intrinsic apoptotic signaling pathway | IGI PMID:16954213 Activation of Ras up-regulates pro-apoptotic BNIP3 in nitric... | KEEP AS NON CORE | Summary: intrinsic apoptotic signaling pathway is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0005515 protein binding | IPI PMID:15235600 RabGEF1 is a negative regulator of mast cell activation and ... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005794 Golgi apparatus | ISS GO_REF:0000024 | ACCEPT | Summary: Golgi apparatus is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005886 plasma membrane | ISS GO_REF:0000024 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0010628 positive regulation of gene expression | IDA PMID:21357543 Regulation of GATA-3 expression during CD4 lineage different... | KEEP AS NON CORE | Summary: positive regulation of gene expression is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0005886 plasma membrane | TAS Reactome:R-MMU-9029152 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005886 plasma membrane | TAS Reactome:R-NUL-1250468 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005886 plasma membrane | TAS Reactome:R-NUL-1250472 | ACCEPT | Summary: plasma membrane is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md dual palmitoylation (C181/C184) supports Golgi retention/exit and cycling to the **plasma membrane** |
| GO:0005515 protein binding | IPI PMID:18604197 IQGAP3 regulates cell proliferation through the Ras/ERK sign... | MARK AS OVER ANNOTATED | Summary: protein binding records a physical association but is too generic to describe the gene product function. Reason: The evidence supports regulated signaling-complex assembly, not a meaningful standalone protein binding function; more informative molecular and pathway terms capture the biology. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0005525 GTP binding | IDA PMID:18604197 IQGAP3 regulates cell proliferation through the Ras/ERK sign... | ACCEPT | Summary: GTP binding is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0097193 intrinsic apoptotic signaling pathway | IMP PMID:16954213 Activation of Ras up-regulates pro-apoptotic BNIP3 in nitric... | KEEP AS NON CORE | Summary: intrinsic apoptotic signaling pathway is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0046579 positive regulation of Ras protein signal transduction | ISO PMID:19029245 The protein phosphatase 2A regulatory subunits B'beta and B'... | ACCEPT | Summary: positive regulation of Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
| GO:0008284 positive regulation of cell population proliferation | IDA PMID:16478791 APC inhibits ERK pathway activation and cellular proliferati... | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0043524 negative regulation of neuron apoptotic process | IDA PMID:10845775 Neurofibromin negatively regulates neurotrophin signaling th... | KEEP AS NON CORE | Summary: negative regulation of neuron apoptotic process is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0043524 negative regulation of neuron apoptotic process | IGI PMID:10845775 Neurofibromin negatively regulates neurotrophin signaling th... | KEEP AS NON CORE | Summary: negative regulation of neuron apoptotic process is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0007264 small GTPase-mediated signal transduction | IDA PMID:14712229 G-protein-coupled receptor-mediated activation of rap GTPase... | MODIFY | Summary: Small GTPase-mediated signaling is correct but less specific than Ras signaling for Hras. Reason: The mouse gene encodes H-Ras, so the Ras protein signal transduction term is more specific. Proposed replacements: Ras protein signal transduction Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse **HRas** encodes a membrane-anchored, Ras-family **small GTPase** that acts as a **signal-transducing molecular switch**. |
| GO:0006897 endocytosis | IDA PMID:12446704 Small GTPase Rah/Rab34 is associated with membrane ruffles a... | KEEP AS NON CORE | Summary: endocytosis is a supported downstream or specialized H-Ras context. Reason: This term reflects a cell-type, disease-model, developmental, transcriptional, or phenotypic consequence of Ras signaling rather than the primary switch function. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Mouse knock-in models demonstrate that **MEK inhibition (PD0325901)** can reverse both signaling readouts and organismal phenotypes |
| GO:0007265 Ras protein signal transduction | TAS PMID:10871846 Targeted deletion of the H-ras gene decreases tumor formatio... | ACCEPT | Summary: Ras protein signal transduction is consistent with core H-Ras switch activity, effector signaling, or localization. Reason: The term directly captures H-Ras guanine nucleotide cycling, membrane localization, or immediate Ras effector pathway output. Supporting Evidence: file:mouse/Hras/Hras-deep-research-falcon.md Active (GTP-bound) HRas recruits and activates multiple effector classes: |
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Download this section (compressed HTML)Q: Which Hras developmental and neuronal annotations reflect direct H-Ras activity versus compensation or redundancy with Nras/Kras?
Q: Should Hras membrane-trafficking annotations distinguish Golgi palmitoylation from plasma-membrane signaling compartments?
Experiment: Quantitatively compare wild-type and palmitoylation-defective H-Ras rescue in Hras/Nras-deficient mouse cells for RAF, PI3K, and RalGEF pathway activation.
Hypothesis: H-Ras pathway output depends on Golgi-plasma membrane cycling and cannot be inferred from generic cytosolic Ras activity.
Type: Allelic rescue and pathway phosphoproteomics
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