Agtr1a encodes the mouse angiotensin II type 1A receptor, a rhodopsin-family GPCR for angiotensin II. The receptor signals mainly through Gq/phospholipase C and calcium mobilization at the plasma membrane and mediates major renin-angiotensin outputs including vasoconstriction, renal sodium/water handling, aldosterone regulation, and blood-pressure control.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0005886 plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: plasma membrane is biologically consistent with the curated synthesis for Agtr1a and is supported by IBA evidence (GO_REF:0000033). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0001822 kidney development | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: kidney development is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse kidney-development evidence: Iosipiv and Schroeder report that "cultured murine UB cells express AT1 receptor protein and mRNA" and that ANG II treatment "elicits a dose-related increase in the number of cells that have primary and secondary branches"; the effect is blocked by the AT1 antagonist candesartan. |
| GO:0008217 regulation of blood pressure | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: regulation of blood pressure is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0038166 angiotensin-activated signaling pathway | IBA GO_REF:0000033 | ACCEPT | Summary: angiotensin-activated signaling pathway is biologically consistent with the curated synthesis for Agtr1a and is supported by IBA evidence (GO_REF:0000033). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0007204 positive regulation of cytosolic calcium ion concentration | IBA GO_REF:0000033 | ACCEPT | Summary: positive regulation of cytosolic calcium ion concentration is biologically consistent with the curated synthesis for Agtr1a and is supported by IBA evidence (GO_REF:0000033). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0001596 angiotensin type I receptor activity | IBA GO_REF:0000033 | ACCEPT | Summary: angiotensin type I receptor activity is biologically consistent with the curated synthesis for Agtr1a and is supported by IBA evidence (GO_REF:0000033). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0006954 inflammatory response | IBA GO_REF:0000033 | MARK AS OVER ANNOTATED | Summary: inflammatory response is a broad downstream phenotype and is not directly established as an Agtr1a-specific annotation by the reviewed evidence. Reason: The curated model is better captured by AT1A receptor activity, angiotensin-activated PLC/calcium signaling, and renal/vascular blood-pressure terms rather than a generic inflammatory-response transfer. Propagation Review Root cause: TERM SCOPING PROBLEM Failure modes: ROLE CONFLATION Sources checked: PANTHER:PTN002796070 SUPPORTS TRANSFER The node is absent from the local PANTHER PAINT cache, so its full IBD seed set could not be inspected; the GOA WITH/FROM lists only the two mouse type-1 angiotensin II receptors, and UniProt classifies the target as PTHR10489:SF956 "TYPE-1 ANGIOTENSIN II RECEPTOR A". Descent of the target from an AT1-receptor node is therefore not in question - the issue is the term chosen, not the node placement. MGI:MGI:87964 · mouse Agtr1a (the review target itself) SUPPORTS TRANSFER The target's own MGI record is one of the two AT1-receptor IBD seeds, so the self-seed marks node membership. It does NOT mark independent experimental grounding here: Agtr1a's own IGI at this same term (GO:0006954, PMID:19404405) is itself reviewed as unsupported in this file, because that study shows the inflammatory effect is preserved when Ang II receptors are absent. Citing it as grounding would lean on an annotation this review removes. MGI:MGI:87965 · mouse Agtr1b (angiotensin II receptor, type 1b) SUPPORTS TRANSFER The closest mouse paralog and the only other seed; AT1a and AT1b share AT1 pharmacology, so transfer between them is sound. What is over-scoped is the term: inflammatory response names a downstream tissue-level consequence of AT1 signalling rather than the receptor's own step in it, which is captured by the angiotensin-activated PLC/calcium and blood-pressure terms retained elsewhere in this review. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0003081 regulation of systemic arterial blood pressure by renin-angiotensin | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: regulation of systemic arterial blood pressure by renin-angiotensin is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0004930 G protein-coupled receptor activity | IEA GO_REF:0000120 | MODIFY | Summary: G protein-coupled receptor activity captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin type I receptor activity for this gene. Replace with angiotensin type I receptor activity to align the annotation with the reviewed evidence. Proposed replacements: angiotensin type I receptor activity Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0004945 angiotensin type II receptor activity | IEA GO_REF:0000002 | MODIFY | Summary: angiotensin type II receptor activity captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin type I receptor activity for this gene. Replace with angiotensin type I receptor activity to align the annotation with the reviewed evidence. Proposed replacements: angiotensin type I receptor activity Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0005886 plasma membrane | IEA GO_REF:0000120 | ACCEPT | Summary: plasma membrane is biologically consistent with the curated synthesis for Agtr1a and is supported by IEA evidence (GO_REF:0000120). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0007165 signal transduction | IEA GO_REF:0000043 | MODIFY | Summary: signal transduction captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin-activated signaling pathway for this gene. Replace with angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0007186 G protein-coupled receptor signaling pathway | IEA GO_REF:0000120 | MODIFY | Summary: G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin-activated signaling pathway for this gene. Replace with angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0016020 membrane | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: membrane is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0019229 regulation of vasoconstriction | IEA GO_REF:0000002 | MODIFY | Summary: regulation of vasoconstriction captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than vasoconstriction for this gene. Replace with vasoconstriction to align the annotation with the reviewed evidence. Proposed replacements: vasoconstriction Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0005515 protein binding | IPI PMID:10358057 Cloning and characterization of ATRAP, a novel protein that ... | MARK AS OVER ANNOTATED | Summary: protein binding is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0005515 protein binding | IPI PMID:15757644 The novel angiotensin II type 1 receptor (AT1R)-associated p... | MARK AS OVER ANNOTATED | Summary: protein binding is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0001596 angiotensin type I receptor activity | IEA GO_REF:0000107 | ACCEPT | Summary: angiotensin type I receptor activity is biologically consistent with the curated synthesis for Agtr1a and is supported by IEA evidence (GO_REF:0000107). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0001921 positive regulation of receptor recycling | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of receptor recycling is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0002018 renin-angiotensin regulation of aldosterone production | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: renin-angiotensin regulation of aldosterone production is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0005794 Golgi apparatus | IEA GO_REF:0000107 | UNDECIDED | Summary: The local evidence supports Agtr1a as a plasma-membrane GPCR but does not verify Golgi localization. Reason: The previous support text described renal blood-pressure physiology and did not justify this specific cellular-component annotation. |
| GO:0006885 regulation of pH | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: regulation of pH is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0007200 phospholipase C-activating G protein-coupled receptor signaling pathway | IEA GO_REF:0000107 | MODIFY | Summary: phospholipase C-activating G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than phospholipase C-activating angiotensin-activated signaling pathway for this gene. Replace with phospholipase C-activating angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: phospholipase C-activating angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0008284 positive regulation of cell population proliferation | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: positive regulation of cell population proliferation is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0009651 response to salt stress | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: response to salt stress is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0014823 response to activity | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: response to activity is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0016323 basolateral plasma membrane | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: basolateral plasma membrane is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0019901 protein kinase binding | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: protein kinase binding is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0030425 dendrite | IEA GO_REF:0000107 | UNDECIDED | Summary: The local evidence supports brain/CNS roles for Agtr1a but does not verify dendrite localization. Reason: Retaining this cellular-component annotation requires direct localization evidence rather than renal or blood-pressure physiology. |
| GO:0031410 cytoplasmic vesicle | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cytoplasmic vesicle is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0031748 D1 dopamine receptor binding | IEA GO_REF:0000107 | REMOVE | Summary: D1 dopamine receptor binding is not supported as an Agtr1a annotation by the reviewed mouse evidence. Reason: The available evidence supports AT1A angiotensin receptor activity; dopamine receptor papers do not establish direct Agtr1a-D1 receptor binding. |
| GO:0031968 organelle outer membrane | IEA GO_REF:0000107 | REMOVE | Summary: organelle outer membrane is not supported as an appropriate annotation for Agtr1a after review of the available mouse evidence. Reason: The term appears to reflect either an unsupported transfer, a paralog/family overreach, or a localization/process inconsistent with the curated Agtr1a biology. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0032930 positive regulation of superoxide anion generation | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: positive regulation of superoxide anion generation is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0038166 angiotensin-activated signaling pathway | IEA GO_REF:0000107 | ACCEPT | Summary: angiotensin-activated signaling pathway is biologically consistent with the curated synthesis for Agtr1a and is supported by IEA evidence (GO_REF:0000107). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0042310 vasoconstriction | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: vasoconstriction is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0042416 dopamine biosynthetic process | IEA GO_REF:0000107 | REMOVE | Summary: dopamine biosynthetic process is not supported as an appropriate annotation for Agtr1a after review of the available mouse evidence. Reason: The term appears to reflect either an unsupported transfer, a paralog/family overreach, or a localization/process inconsistent with the curated Agtr1a biology. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0042756 drinking behavior | IEA GO_REF:0000120 | REMOVE | Summary: Drinking behavior is not supported as an Agtr1a-specific annotation by the reviewed mouse evidence. Reason: Direct central angiotensin II experiments separate AT1A-dependent blood-pressure responses from drinking behavior, which requires AT1B. Supporting Evidence: PMID:10880053 the drinking response requires the presence of AT(1B) receptors. |
| GO:0043627 response to estrogen | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: response to estrogen is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0045766 positive regulation of angiogenesis | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: positive regulation of angiogenesis is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0045777 positive regulation of blood pressure | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of blood pressure is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0051412 response to corticosterone | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: response to corticosterone is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0055037 recycling endosome | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: recycling endosome is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0071549 cellular response to dexamethasone stimulus | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: cellular response to dexamethasone stimulus is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0090190 positive regulation of branching involved in ureteric bud morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of branching involved in ureteric bud morphogenesis is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse kidney-development evidence: Iosipiv and Schroeder report that "cultured murine UB cells express AT1 receptor protein and mRNA" and that ANG II treatment "elicits a dose-related increase in the number of cells that have primary and secondary branches"; the effect is blocked by the AT1 antagonist candesartan. |
| GO:1905665 positive regulation of calcium ion import across plasma membrane | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of calcium ion import across plasma membrane is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:1990776 response to angiotensin | IEA GO_REF:0000107 | MODIFY | Summary: response to angiotensin captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin-activated signaling pathway for this gene. Replace with angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0042976 activation of Janus kinase activity | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: activation of Janus kinase activity is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0001596 angiotensin type I receptor activity | ISO GO_REF:0000096 | ACCEPT | Summary: angiotensin type I receptor activity is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000096). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0001596 angiotensin type I receptor activity | ISO GO_REF:0000119 | ACCEPT | Summary: angiotensin type I receptor activity is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000119). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0001822 kidney development | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: kidney development is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse kidney-development evidence: Iosipiv and Schroeder report that "cultured murine UB cells express AT1 receptor protein and mRNA" and that ANG II treatment "elicits a dose-related increase in the number of cells that have primary and secondary branches"; the effect is blocked by the AT1 antagonist candesartan. |
| GO:0001921 positive regulation of receptor recycling | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: positive regulation of receptor recycling is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0002018 renin-angiotensin regulation of aldosterone production | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: renin-angiotensin regulation of aldosterone production is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0002034 maintenance of blood vessel diameter homeostasis by renin-angiotensin | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: maintenance of blood vessel diameter homeostasis by renin-angiotensin is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0004945 angiotensin type II receptor activity | ISO GO_REF:0000119 | MODIFY | Summary: angiotensin type II receptor activity captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin type I receptor activity for this gene. Replace with angiotensin type I receptor activity to align the annotation with the reviewed evidence. Proposed replacements: angiotensin type I receptor activity Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0005794 Golgi apparatus | ISO GO_REF:0000096 | UNDECIDED | Summary: The local evidence supports Agtr1a as a plasma-membrane GPCR but does not verify Golgi localization. Reason: The previous support text described renal blood-pressure physiology and did not justify this specific cellular-component annotation. |
| GO:0005886 plasma membrane | ISO GO_REF:0000096 | ACCEPT | Summary: plasma membrane is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000096). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0005886 plasma membrane | ISO GO_REF:0000119 | ACCEPT | Summary: plasma membrane is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000119). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0006885 regulation of pH | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: regulation of pH is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0007186 G protein-coupled receptor signaling pathway | ISO GO_REF:0000096 | MODIFY | Summary: G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin-activated signaling pathway for this gene. Replace with angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0007186 G protein-coupled receptor signaling pathway | ISO GO_REF:0000119 | MODIFY | Summary: G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin-activated signaling pathway for this gene. Replace with angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0007200 phospholipase C-activating G protein-coupled receptor signaling pathway | ISO GO_REF:0000096 | MODIFY | Summary: phospholipase C-activating G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than phospholipase C-activating angiotensin-activated signaling pathway for this gene. Replace with phospholipase C-activating angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: phospholipase C-activating angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0007200 phospholipase C-activating G protein-coupled receptor signaling pathway | ISO GO_REF:0000119 | MODIFY | Summary: phospholipase C-activating G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than phospholipase C-activating angiotensin-activated signaling pathway for this gene. Replace with phospholipase C-activating angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: phospholipase C-activating angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0007204 positive regulation of cytosolic calcium ion concentration | ISO GO_REF:0000119 | ACCEPT | Summary: positive regulation of cytosolic calcium ion concentration is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000119). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0007266 Rho protein signal transduction | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: Rho protein signal transduction is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0008284 positive regulation of cell population proliferation | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: positive regulation of cell population proliferation is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0010744 positive regulation of macrophage derived foam cell differentiation | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: positive regulation of macrophage derived foam cell differentiation is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0016323 basolateral plasma membrane | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: basolateral plasma membrane is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0019229 regulation of vasoconstriction | ISO GO_REF:0000119 | MODIFY | Summary: regulation of vasoconstriction captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than vasoconstriction for this gene. Replace with vasoconstriction to align the annotation with the reviewed evidence. Proposed replacements: vasoconstriction Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0019722 calcium-mediated signaling | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: calcium-mediated signaling is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0019901 protein kinase binding | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: protein kinase binding is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0030425 dendrite | ISO GO_REF:0000096 | UNDECIDED | Summary: The local evidence supports brain/CNS roles for Agtr1a but does not verify dendrite localization. Reason: Retaining this cellular-component annotation requires direct localization evidence rather than renal or blood-pressure physiology. |
| GO:0031410 cytoplasmic vesicle | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: cytoplasmic vesicle is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0031711 bradykinin receptor binding | ISO GO_REF:0000119 | KEEP AS NON CORE | Summary: bradykinin receptor binding is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0031748 D1 dopamine receptor binding | ISO GO_REF:0000096 | REMOVE | Summary: D1 dopamine receptor binding is not supported as an Agtr1a annotation by the reviewed mouse evidence. Reason: The available evidence supports AT1A angiotensin receptor activity; dopamine receptor papers do not establish direct Agtr1a-D1 receptor binding. |
| GO:0031968 organelle outer membrane | ISO GO_REF:0000096 | REMOVE | Summary: organelle outer membrane is not supported as an appropriate annotation for Agtr1a after review of the available mouse evidence. Reason: The term appears to reflect either an unsupported transfer, a paralog/family overreach, or a localization/process inconsistent with the curated Agtr1a biology. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0032930 positive regulation of superoxide anion generation | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: positive regulation of superoxide anion generation is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0038166 angiotensin-activated signaling pathway | ISO GO_REF:0000096 | ACCEPT | Summary: angiotensin-activated signaling pathway is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000096). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0038166 angiotensin-activated signaling pathway | ISO GO_REF:0000119 | ACCEPT | Summary: angiotensin-activated signaling pathway is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000119). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0042310 vasoconstriction | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: vasoconstriction is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0042416 dopamine biosynthetic process | ISO GO_REF:0000096 | REMOVE | Summary: dopamine biosynthetic process is not supported as an appropriate annotation for Agtr1a after review of the available mouse evidence. Reason: The term appears to reflect either an unsupported transfer, a paralog/family overreach, or a localization/process inconsistent with the curated Agtr1a biology. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0042756 drinking behavior | ISO GO_REF:0000096 | REMOVE | Summary: Drinking behavior is not supported as an Agtr1a-specific annotation by the reviewed mouse evidence. Reason: Direct central angiotensin II experiments separate AT1A-dependent blood-pressure responses from drinking behavior, which requires AT1B. Supporting Evidence: PMID:10880053 the drinking response requires the presence of AT(1B) receptors. |
| GO:0043627 response to estrogen | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: response to estrogen is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0045766 positive regulation of angiogenesis | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: positive regulation of angiogenesis is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0045777 positive regulation of blood pressure | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: positive regulation of blood pressure is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0046718 symbiont entry into host cell | ISO GO_REF:0000119 | REMOVE | Summary: symbiont entry into host cell is not supported as an appropriate annotation for Agtr1a after review of the available mouse evidence. Reason: The term appears to reflect either an unsupported transfer, a paralog/family overreach, or a localization/process inconsistent with the curated Agtr1a biology. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0046982 protein heterodimerization activity | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: protein heterodimerization activity is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0055037 recycling endosome | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: recycling endosome is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0060326 cell chemotaxis | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: cell chemotaxis is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0071549 cellular response to dexamethasone stimulus | ISO GO_REF:0000096 | MARK AS OVER ANNOTATED | Summary: cellular response to dexamethasone stimulus is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0086097 phospholipase C-activating angiotensin-activated signaling pathway | ISO GO_REF:0000119 | ACCEPT | Summary: phospholipase C-activating angiotensin-activated signaling pathway is biologically consistent with the curated synthesis for Agtr1a and is supported by ISO evidence (GO_REF:0000119). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
| GO:0090190 positive regulation of branching involved in ureteric bud morphogenesis | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: positive regulation of branching involved in ureteric bud morphogenesis is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse kidney-development evidence: Iosipiv and Schroeder report that "cultured murine UB cells express AT1 receptor protein and mRNA" and that ANG II treatment "elicits a dose-related increase in the number of cells that have primary and secondary branches"; the effect is blocked by the AT1 antagonist candesartan. |
| GO:0090205 positive regulation of cholesterol metabolic process | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: positive regulation of cholesterol metabolic process is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:1903589 positive regulation of blood vessel endothelial cell proliferation involved in sprouting angiogenesis | ISO GO_REF:0000119 | MARK AS OVER ANNOTATED | Summary: positive regulation of blood vessel endothelial cell proliferation involved in sprouting angiogenesis is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:1905665 positive regulation of calcium ion import across plasma membrane | ISO GO_REF:0000096 | KEEP AS NON CORE | Summary: positive regulation of calcium ion import across plasma membrane is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0010467 gene expression | IMP PMID:24206662 Mineralocorticoid receptor phosphorylation regulates ligand ... | KEEP AS NON CORE | Summary: gene expression is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0002034 maintenance of blood vessel diameter homeostasis by renin-angiotensin | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: maintenance of blood vessel diameter homeostasis by renin-angiotensin is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0008217 regulation of blood pressure | IMP PMID:26531127 Age-dependent blood pressure elevation is due to increased v... | KEEP AS NON CORE | Summary: regulation of blood pressure is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0006954 inflammatory response | IGI PMID:19404405 Angiotensin-(1-7) and the g protein-coupled receptor MAS are... | REMOVE | Summary: This paper supports Mas/Ang-(1-7)-dependent renal inflammation, not an Agtr1a-specific inflammatory response. Reason: The cited study explicitly shows the inflammatory effect is preserved when Ang II receptors are absent, so it should not be retained for Agtr1a. Supporting Evidence: PMID:19404405 showing that this effect is AT1 and AT2 independent |
| GO:0034391 regulation of smooth muscle cell apoptotic process | IGI PMID:19508861 The heterogenous nuclear riboprotein S1-1 regulates AT1 rece... | KEEP AS NON CORE | Summary: regulation of smooth muscle cell apoptotic process is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0034392 negative regulation of smooth muscle cell apoptotic process | IMP PMID:19508861 The heterogenous nuclear riboprotein S1-1 regulates AT1 rece... | KEEP AS NON CORE | Summary: negative regulation of smooth muscle cell apoptotic process is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0008284 positive regulation of cell population proliferation | IMP PMID:19508861 The heterogenous nuclear riboprotein S1-1 regulates AT1 rece... | MARK AS OVER ANNOTATED | Summary: positive regulation of cell population proliferation is related to reported Agtr1a biology only as a broad downstream readout or generic interaction term. Reason: This overstates the direct role of the gene product; the curated model is better captured by the specific receptor/ligand, pathway, and supported non-core phenotype terms. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Curation judgment: terms that describe broad responses to hormones, salt, activity, estrogen, corticosterone, dexamethasone, or generic cell proliferation/inflammation are generally downstream, context-specific phenotypes of angiotensin signaling. |
| GO:0002035 brain renin-angiotensin system | IMP PMID:16585392 Role of p90 ribosomal S6 kinase-mediated prorenin-converting... | KEEP AS NON CORE | Summary: brain renin-angiotensin system is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0007507 heart development | IMP PMID:16585392 Role of p90 ribosomal S6 kinase-mediated prorenin-converting... | KEEP AS NON CORE | Summary: heart development is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0001819 positive regulation of cytokine production | IMP PMID:19023134 Serotonin and angiotensin receptors in cardiac fibroblasts c... | KEEP AS NON CORE | Summary: positive regulation of cytokine production is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0045777 positive regulation of blood pressure | IMP PMID:12486173 Mice lacking D5 dopamine receptors have increased sympatheti... | UNDECIDED | Summary: Cannot be adjudicated here: PMID:12486173 is cached abstract-only. Prior observation, not a verdict: This dopamine D5 receptor paper does not establish a direct Agtr1a positive regulation of blood pressure annotation. Reason: PMID:12486173 is cached abstract-only, so the curator's experimental evidence cannot be inspected here; per CLAUDE.md an experimental annotation is not overruled on that basis. Recorded observation, not a verdict: Other direct Agtr1a blood-pressure annotations are retained, but this source-specific row is based on a dopamine receptor knockout study rather than Agtr1a function. Supporting Evidence: PMID:12486173 Mice lacking D5 dopamine receptors have increased sympathetic tone and are hypertensive. |
| GO:0045777 positive regulation of blood pressure | IGI PMID:9691085 Disruption of the dopamine D3 receptor gene produces renin-d... | UNDECIDED | Summary: Cannot be adjudicated here: PMID:9691085 is cached abstract-only. Prior observation, not a verdict: This dopamine D3 receptor paper does not establish a direct Agtr1a positive regulation of blood pressure annotation. Reason: PMID:9691085 is cached abstract-only, so the curator's experimental evidence cannot be inspected here; per CLAUDE.md an experimental annotation is not overruled on that basis. Recorded observation, not a verdict: Other direct Agtr1a blood-pressure annotations are retained, but this source-specific row is based on a dopamine receptor knockout study rather than Agtr1a function. Supporting Evidence: PMID:9691085 disruption of the D3 receptor, a member of the family of D2-like receptors |
| GO:0045777 positive regulation of blood pressure | IDA PMID:12486173 Mice lacking D5 dopamine receptors have increased sympatheti... | UNDECIDED | Summary: Cannot be adjudicated here: PMID:12486173 is cached abstract-only. Prior observation, not a verdict: This dopamine D5 receptor paper does not establish a direct Agtr1a positive regulation of blood pressure annotation. Reason: PMID:12486173 is cached abstract-only, so the curator's experimental evidence cannot be inspected here; per CLAUDE.md an experimental annotation is not overruled on that basis. Recorded observation, not a verdict: Other direct Agtr1a blood-pressure annotations are retained, but this source-specific row is based on a dopamine receptor knockout study rather than Agtr1a function. Supporting Evidence: PMID:12486173 Mice lacking D5 dopamine receptors have increased sympathetic tone and are hypertensive. |
| GO:0005737 cytoplasm | IDA PMID:15499027 Angiotensin II impairs neurovascular coupling in neocortex t... | UNDECIDED | Summary: The cited cerebral microvessel paper supports AT1 localization in vascular cells but does not verify cytoplasm as the appropriate component. Reason: Agtr1a is retained as a membrane GPCR; a cytoplasm annotation needs term-specific localization evidence rather than vascular physiology. |
| GO:0005886 plasma membrane | IDA PMID:15499027 Angiotensin II impairs neurovascular coupling in neocortex t... | ACCEPT | Summary: plasma membrane is biologically consistent with the curated synthesis for Agtr1a and is supported by IDA evidence (PMID:15499027). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0001568 blood vessel development | IGI PMID:9466969 Murine double nullizygotes of the angiotensin type 1A and 1B... | KEEP AS NON CORE | Summary: blood vessel development is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0001822 kidney development | IMP PMID:12167595 Effects of AT(1A) receptor deletion on blood pressure and so... | KEEP AS NON CORE | Summary: kidney development is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse kidney-development evidence: Iosipiv and Schroeder report that "cultured murine UB cells express AT1 receptor protein and mRNA" and that ANG II treatment "elicits a dose-related increase in the number of cells that have primary and secondary branches"; the effect is blocked by the AT1 antagonist candesartan. |
| GO:0001822 kidney development | IGI PMID:9466969 Murine double nullizygotes of the angiotensin type 1A and 1B... | KEEP AS NON CORE | Summary: kidney development is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse kidney-development evidence: Iosipiv and Schroeder report that "cultured murine UB cells express AT1 receptor protein and mRNA" and that ANG II treatment "elicits a dose-related increase in the number of cells that have primary and secondary branches"; the effect is blocked by the AT1 antagonist candesartan. |
| GO:0001991 regulation of systemic arterial blood pressure by circulatory renin-angiotensin | IGI PMID:9466969 Murine double nullizygotes of the angiotensin type 1A and 1B... | KEEP AS NON CORE | Summary: regulation of systemic arterial blood pressure by circulatory renin-angiotensin is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0002001 renin secretion into blood stream | IMP PMID:12167595 Effects of AT(1A) receptor deletion on blood pressure and so... | KEEP AS NON CORE | Summary: renin secretion into blood stream is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0002018 renin-angiotensin regulation of aldosterone production | IMP PMID:12167595 Effects of AT(1A) receptor deletion on blood pressure and so... | KEEP AS NON CORE | Summary: renin-angiotensin regulation of aldosterone production is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0002019 regulation of renal output by angiotensin | IMP PMID:12167595 Effects of AT(1A) receptor deletion on blood pressure and so... | KEEP AS NON CORE | Summary: regulation of renal output by angiotensin is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Mouse renal and blood-pressure physiology: AT1A-deficient mice on altered salt diets show "high urinary volume and low blood pressure despite increased renin and aldosterone levels" and a shifted pressure-natriuresis relationship. |
| GO:0042756 drinking behavior | IMP PMID:12167595 Effects of AT(1A) receptor deletion on blood pressure and so... | UNDECIDED | Summary: Cannot be adjudicated here: PMID:12167595 is cached abstract-only. Prior observation, not a verdict: This renal sodium-balance paper does not support drinking behavior as an Agtr1a-specific annotation. Reason: PMID:12167595 is cached abstract-only, so the curator's experimental evidence cannot be inspected here; per CLAUDE.md an experimental annotation is not overruled on that basis. Recorded observation, not a verdict: The cited study supports renal output and blood-pressure physiology; direct central angiotensin II evidence instead assigns drinking behavior primarily to AT1B rather than AT1A. Supporting Evidence: PMID:12167595 These studies demonstrate that mice lacking the AT(1A) receptor have blood pressures sensitive to changes in dietary sodium |
| GO:0001596 angiotensin type I receptor activity | IDA PMID:12657564 A role for angiotensin II AT1 receptors in ureteric bud cell... | ACCEPT | Summary: angiotensin type I receptor activity is biologically consistent with the curated synthesis for Agtr1a and is supported by IDA evidence (PMID:12657564). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. file:mouse/Agtr1a/Agtr1a-deep-research-falcon.md Agtr1a encodes a **cell-surface receptor** whose primary function is to **bind Ang II** and transduce signals through: |
| GO:0002035 brain renin-angiotensin system | IMP PMID:10880053 Divergent functions of angiotensin II receptor isoforms in t... | KEEP AS NON CORE | Summary: brain renin-angiotensin system is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: PMID:10880053 AT(1A) expression generally exceeding AT(1B) expression |
| GO:0042756 drinking behavior | IMP PMID:10880053 Divergent functions of angiotensin II receptor isoforms in t... | UNDECIDED | Summary: Cannot be adjudicated here: PMID:10880053 is cached abstract-only. Prior observation, not a verdict: Drinking behavior is not supported as an Agtr1a-specific annotation by this direct central angiotensin II study. Reason: PMID:10880053 is cached abstract-only, so the curator's experimental evidence cannot be inspected here; per CLAUDE.md an experimental annotation is not overruled on that basis. Recorded observation, not a verdict: The same citation explicitly separates AT1A-dependent blood-pressure responses from drinking behavior, which requires AT1B. Supporting Evidence: PMID:10880053 the drinking response requires the presence of AT(1B) receptors. |
| GO:0042756 drinking behavior | IGI PMID:10880053 Divergent functions of angiotensin II receptor isoforms in t... | UNDECIDED | Summary: Cannot be adjudicated here: PMID:10880053 is cached abstract-only. Prior observation, not a verdict: Drinking behavior is not supported as an Agtr1a-specific annotation by this direct central angiotensin II study. Reason: PMID:10880053 is cached abstract-only, so the curator's experimental evidence cannot be inspected here; per CLAUDE.md an experimental annotation is not overruled on that basis. Recorded observation, not a verdict: The same citation explicitly separates AT1A-dependent blood-pressure responses from drinking behavior, which requires AT1B. Supporting Evidence: PMID:10880053 the drinking response requires the presence of AT(1B) receptors. |
| GO:0005768 endosome | IDA PMID:14718562 Phospholipase D2 localizes to the plasma membrane and regula... | KEEP AS NON CORE | Summary: endosome is supported for Agtr1a in a tissue, developmental, trafficking, or disease-model context, but it is not the core molecular role. Reason: This annotation captures a real downstream or context-specific consequence of Agtr1a activity. It should be retained as non-core so it does not obscure the primary receptor/ligand signaling function. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Trafficking and protein-interaction evidence: ATRAP was isolated using the cytoplasmic domain of murine AT1A and "interacts specifically with the carboxyl-terminal domain of the AT1a receptor"; overexpression inhibits AT1A-mediated PLC activation. |
| GO:0005886 plasma membrane | IDA PMID:14718562 Phospholipase D2 localizes to the plasma membrane and regula... | ACCEPT | Summary: plasma membrane is biologically consistent with the curated synthesis for Agtr1a and is supported by IDA evidence (PMID:14718562). Reason: The term matches a direct molecular function, pathway, or location/physiological output of Agtr1a; it is specific enough to retain without replacement. Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core receptor identity: Agtr1a encodes the mouse type-1 angiotensin II receptor A, a seven-transmembrane G protein-coupled receptor whose primary molecular function is angiotensin type I receptor activity. |
| GO:0007186 G protein-coupled receptor signaling pathway | IC PMID:12657564 A role for angiotensin II AT1 receptors in ureteric bud cell... | MODIFY | Summary: G protein-coupled receptor signaling pathway captures the right general biology for Agtr1a, but a more specific GO term is available. Reason: The current term is too broad or less precise than angiotensin-activated signaling pathway for this gene. Replace with angiotensin-activated signaling pathway to align the annotation with the reviewed evidence. Proposed replacements: angiotensin-activated signaling pathway Supporting Evidence: file:mouse/Agtr1a/Agtr1a-notes.md Core signaling: UniProt states that activated AGTR1A "couples to G-alpha proteins G(q) (GNAQ, GNA11, GNA14 or GNA15) and thus activates phospholipase C and increases the cytosolic Ca(2+) concentrations." |
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Download this section (compressed HTML)Q: Which mouse AGTR1A signaling outputs should be represented as direct receptor signaling annotations rather than downstream organismal blood-pressure or kidney phenotypes?
Experiment: Measure Ang II-induced PLC activation, calcium mobilization, and ERK/Rho pathway activation in Agtr1a-null and rescued mouse cells, including antagonist controls and Agtr1b comparison.
Hypothesis: The clearest direct AGTR1A pathway annotation is Gq/PLC/calcium signaling downstream of angiotensin II.
Type: cell signaling rescue assay
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