BMPR1A (ALK3) is a single-pass cell-surface BMP receptor with an extracellular ligand-binding domain and an intracellular serine/threonine kinase domain. It recognizes BMP-family ligands in complexes with type II receptors; activation of its kinase couples extracellular signals to receptor-regulated SMADs. Ligand preference and output depend on receptor partners and cellular context. This signaling supports skeletal and cardiovascular development, differentiation and hepatic hepcidin regulation. BMPR1A also supplies type I receptor signaling in the AMH pathway during MΓΌllerian-duct regression.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0001525 angiogenesis | IMP PMID:24882581 MicroRNA-885-3p inhibits the growth of HT-29 colon cancer ce... | KEEP AS NON CORE | Summary: BMPR1A-dependent BMP signaling supports angiogenesis in the HT-29 tumor model (PMID:24882581). Reason: The perturbation study connects BMPR1A/BMP/SMAD/ID1 signaling to vascularization of colon-cancer xenografts. Retain this experimental process assertion in its tumor context; the defining molecular activity is receptor kinase signaling, rather than an angiogenesis-specific enzyme. |
| GO:0001649 osteoblast differentiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse orthology supports an osteoblast-differentiation role of human BMPR1A. Reason: The GO_REF:0000107 transfer from mouse P36895 is consistent with human mesenchymal-cell receptor perturbation in PMID:18436533. Retain the developmental outcome as non-core; the receptor transduces BMP signals rather than executing the osteoblast transcriptional program itself. |
| GO:0002062 chondrocyte differentiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: BMPR1A-mediated GDF5 signaling contributes to chondrocyte differentiation. Reason: The mouse orthology transfer is compatible with the GDF5 receptor function summarized in UniProt and the ligand/receptor experiments of PMID:24098149. GDF5 preference for BMPR1B does not eliminate lower-affinity BMPR1A binding. Retain this tissue-specific consequence of receptor activity. |
| GO:0003148 outflow tract septum morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports outflow-tract septation downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for separation and remodeling of the embryonic cardiac outflow tract. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003148 outflow tract septum morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports outflow-tract septation downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for separation and remodeling of the embryonic cardiac outflow tract. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003151 outflow tract morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports outflow-tract morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for formation and remodeling of the embryonic cardiac outflow tract. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003151 outflow tract morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports outflow-tract morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for formation and remodeling of the embryonic cardiac outflow tract. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003161 cardiac conduction system development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports cardiac conduction-system development downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for specialization of cardiac conduction tissue. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003161 cardiac conduction system development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports cardiac conduction-system development downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for specialization of cardiac conduction tissue. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003171 atrioventricular valve development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports atrioventricular valve development downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for development of the atrioventricular valves. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003171 atrioventricular valve development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports atrioventricular valve development downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for development of the atrioventricular valves. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003183 mitral valve morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports mitral-valve morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for left atrioventricular valve morphogenesis. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003183 mitral valve morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports mitral-valve morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for left atrioventricular valve morphogenesis. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003186 tricuspid valve morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports tricuspid-valve morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for right atrioventricular valve morphogenesis. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003186 tricuspid valve morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports tricuspid-valve morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for right atrioventricular valve morphogenesis. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003203 endocardial cushion morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports endocardial-cushion morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for remodeling of endocardial cushion tissue. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003203 endocardial cushion morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports endocardial-cushion morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for remodeling of endocardial cushion tissue. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003215 cardiac right ventricle morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports right-ventricular morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for embryonic right-ventricular development. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003215 cardiac right ventricle morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports right-ventricular morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for embryonic right-ventricular development. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0003222 ventricular trabecula myocardium morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports ventricular trabecular-myocardium morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for development of the trabecular ventricular myocardium. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0003222 ventricular trabecula myocardium morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports ventricular trabecular-myocardium morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for development of the trabecular ventricular myocardium. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0003223 ventricular compact myocardium morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports compact-myocardium morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for growth of the compact ventricular myocardium. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0003223 ventricular compact myocardium morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports compact-myocardium morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for growth of the compact ventricular myocardium. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0003272 endocardial cushion formation | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports endocardial-cushion formation downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for initial formation of the endocardial cushions. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0004672 protein kinase activity | IEA GO_REF:0000002 | ACCEPT | Summary: BMPR1A has intrinsic protein kinase activity. Reason: The InterPro-derived kinase annotation fits the cytoplasmic catalytic domain and established type I receptor phosphorylation mechanism. The broader term is correct alongside the more specific receptor serine/threonine kinase and BMP receptor terms; it need not be deleted as redundant. |
| GO:0004674 protein serine/threonine kinase activity | IDA PMID:12065756 SB-431542 is a potent and specific inhibitor of transforming... | ACCEPT | Summary: BMPR1A is a catalytically active serine/threonine kinase (PMID:12065756). Reason: The inhibitor paper includes BMP-receptor comparators, and indexed publisher Methods identify activated human ALK3. Its ALK4/5/7-focused title is not a wrong-gene argument. Retain the established kinase activity with curator deference; the original construct-specific biochemical results were not independently read in full. |
| GO:0004675 transmembrane receptor protein serine/threonine kinase activity | IEA GO_REF:0000120 | ACCEPT | Summary: BMPR1A is a transmembrane receptor serine/threonine kinase. Reason: The integrated electronic annotation matches the ligand-binding extracellular domain, single membrane helix and intracellular kinase domain of human P36894. Type II receptors activate the type I receptor, which supplies the subsequent SMAD-directed catalytic step. |
| GO:0004675 transmembrane receptor protein serine/threonine kinase activity | TAS Reactome:R-HSA-201476 | ACCEPT | Summary: Activated BMPR1A performs the type I receptor kinase step upstream of SMADs. Reason: R-HSA-201476 explicitly describes phosphorylation of R-SMAD1/5/8 by activated type I receptors. This is BMPR1A catalytic activity, distinct from the upstream phosphorylation of BMPR1A by a type II receptor. |
| GO:0005025 transforming growth factor beta receptor activity, type I | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: The PAINT assertion uses the conventional TGF-beta-superfamily type I receptor designation. Reason: PANTHER:PTN000584016 records a curator phylogenetic inference; target P36894 among its supporting entities is legitimate experimental grounding, not circularity. All six cached BMPR1A GO-CAM activities also use GO:0005025. Retain this curated usage, while using GO:0098821 BMP receptor activity for the core and flagging the current ligand-specific term definition for clarification. It should not be read as new evidence for direct TGF-beta-ligand binding. |
| GO:0005025 transforming growth factor beta receptor activity, type I | IDA PMID:9136927 The TGF-beta family mediator Smad1 is phosphorylated directl... | KEEP AS NON CORE | Summary: BMPR1A is the BMP type I receptor represented by this experimental type I receptor annotation. Reason: PMID:9136927 establishes receptor-dependent direct SMAD1 phosphorylation; the exact construct-specific full text was not independently retrieved. The same evidence is repeatedly used for BMPR1A in curated GO-CAMs. Preserve the assertion with curator deference, distinguish the broad superfamily convention from specific TGF-beta ligand reception, and synthesize the established BMP receptor activity separately. |
| GO:0005515 protein binding | IPI PMID:10881198 Crystal structure of the BMP-2-BRIA ectodomain complex. | MODIFY | Summary: The BMP2 partner identifies a specific ligand-binding activity (PMID:10881198). Reason: The abstract directly describes human dimeric BMP2 complexed with BMPR1A extracellular domains. Replace generic protein binding with BMP binding; preserve partner P12643. Ligand contacts do not establish direct contact between receptor ectodomains. Proposed replacements: BMP binding Supporting Evidence: PMID:10881198 complex with two high affinity BMP receptor IA extracellular domains |
| GO:0005515 protein binding | IPI PMID:11278302 Transforming growth factor-beta receptor-associated protein ... | UNDECIDED | Summary: The particular BMPR1AβTGFBRAP1 interaction requires source-level confirmation. Reason: PMID:11278302 focuses on TGFBRAP1/TRAP1 as a SMAD4 chaperone; the accessible abstract does not resolve the experiment underlying the BMPR1AβQ8WUH2 assertion. Preserve the curated interaction and partner pending full-text verification. This is not a finding of paralog confusion, nor evidence that BMPR1A itself is a chaperone. |
| GO:0005515 protein binding | IPI PMID:15064755 Molecular recognition of BMP-2 and BMP receptor IA. | MODIFY | Summary: The BMP2βBMPR1A interface supports BMP binding (PMID:15064755). Reason: Mutational and structural analysis identifies the BMP2/BRIA binding interface, including the ligand L51P loss of type I receptor binding. GO:0036122 describes the retained P12643 interaction more precisely than generic protein binding. Proposed replacements: BMP binding Supporting Evidence: PMID:15064755 epitopes of BMP-2 and the BRIA receptor form a new type of protein-protein interface |
| GO:0005515 protein binding | IPI PMID:16127465 Activating and deactivating mutations in the receptor intera... | MODIFY | Summary: BMPR1A binds the BMP-family ligand GDF5 with variant-dependent affinity. Reason: PMID:16127465 compares wild-type and mutant GDF5 binding to BMPR1A and BMPR1B ectodomains. The GDF5 variants alter receptor affinity; they are not BMPR1A isoforms. Preserve P43026 and refine to BMP binding without equating BMPR1A affinity with the preferred BMPR1B interaction. Proposed replacements: BMP binding Supporting Evidence: PMID:16127465 increased binding to BMPR1A |
| GO:0005515 protein binding | IPI PMID:16672363 Structure of the ternary signaling complex of a TGF-beta sup... | MODIFY | Summary: The ternary BMP2 receptor structure supports BMP binding by BMPR1A. Reason: PMID:16672363 directly places BMPR1A ectodomains against the BMP2 ligand in the type I/type II assembly. Refine the P12643 interaction to BMP binding; the structure explicitly separates the receptor ectodomain interfaces and does not establish direct type Iβtype II ectodomain binding. Proposed replacements: BMP binding Supporting Evidence: PMID:16672363 its type I receptor [bone morphogenetic protein receptor type Ia (BMPR-Ia)-ECD] |
| GO:0005515 protein binding | IPI PMID:18436533 BMP-2/4 and BMP-6/7 differentially utilize cell surface rece... | KEEP AS NON CORE | Summary: Full-length BMPR1A associates with ACVR1 in receptor-complex experiments. Reason: PMID:18436533 uses human receptor fusion constructs in HEK-293 BRET saturation/competition experiments, supporting association with ACVR1/Q04771. Retain the interaction as non-core: this is not a purified pairwise binding or fixed-stoichiometry measurement, and no more specific molecular activity follows from the association alone. The scoped retention preserves supported biology despite the repository preference for more informative binding terms. |
| GO:0005515 protein binding | IPI PMID:19229295 Crystal structure analysis reveals a spring-loaded latch as ... | MODIFY | Summary: GDF5 binding is compatible with a lower-affinity BMPR1A interaction. Reason: PMID:19229295 contrasts receptor-binding surfaces and GDF5 preference for BMPR1B; it does not establish complete absence of BMPR1A binding. Combined with direct comparisons in PMID:16127465 and PMID:24098149, the P43026 assertion can be refined to BMP binding. Preserve ligand- and variant-dependent affinity rather than transfer BMPR1B high affinity to BMPR1A. Proposed replacements: BMP binding Supporting Evidence: PMID:19229295 GDF-5-mediated signal transduction involves both BMP type I receptors, BMPR-IA and BMPR-IB |
| GO:0005515 protein binding | IPI PMID:19804412 The pro-form of BMP-2 interferes with BMP-2 signalling by co... | MODIFY | Summary: ProBMP2 binds the BMPR1A extracellular domain without mature-ligand-like activation. Reason: PMID:19804412 directly measures proBMP2 binding to purified BMPR1A ectodomain and cell-surface receptor. Refine P12643 protein binding to BMP binding, explicitly retaining the pro-form condition. Binding in this experiment does not imply osteogenic agonism or the signaling potency of mature BMP2. Proposed replacements: BMP binding Supporting Evidence: PMID:19804412 ProBMP-2 was found to bind to the purified extracellular ligand binding domain (ECD) of BMPR-IA |
| GO:0005515 protein binding | IPI PMID:20860622 DIP2 disco-interacting protein 2 homolog A (Drosophila) is a... | MODIFY | Summary: BMP2 binding to BMPR1A supports a specific BMP-binding annotation. Reason: Publisher Results and Figure 8J/K of PMID:20860622 report BMP2 binding to soluble BMPR1A during sequential SPR experiments with FSTL1. Refine to BMP binding, preserving the ligand accession. This measures ligand recognition, without establishing full-length receptor signaling or physiological affinity. Proposed replacements: BMP binding |
| GO:0005515 protein binding | IPI PMID:20860622 DIP2 disco-interacting protein 2 homolog A (Drosophila) is a... | MODIFY | Summary: BMP4 binding to BMPR1A supports a specific BMP-binding annotation. Reason: Publisher Results and Figure 8J/K of PMID:20860622 report BMP4 binding to soluble BMPR1A during sequential SPR experiments with FSTL1. Refine to BMP binding, preserving the ligand accession. This measures ligand recognition, without establishing full-length receptor signaling or physiological affinity. Proposed replacements: BMP binding |
| GO:0005515 protein binding | IPI PMID:21054789 WFIKKN1 and WFIKKN2 bind growth factors TGFΞ²1, BMP2 and BMP4... | MODIFY | Summary: BMP2 binding to BMPR1A supports a specific BMP-binding annotation. Reason: PMID:21054789 Figure 3A/B and Methods directly test BMP2 binding to recombinant human BMPR1A ectodomain by SPR. Refine to BMP binding while preserving the ligand accession. The purified ectodomain experiment does not by itself establish signaling by the intact receptor. Proposed replacements: BMP binding |
| GO:0005515 protein binding | IPI PMID:21054789 WFIKKN1 and WFIKKN2 bind growth factors TGFΞ²1, BMP2 and BMP4... | MODIFY | Summary: BMP4 binding to BMPR1A supports a specific BMP-binding annotation. Reason: PMID:21054789 Figure 3A/B and Methods directly test BMP4 binding to recombinant human BMPR1A ectodomain by SPR. Refine to BMP binding while preserving the ligand accession. The purified ectodomain experiment does not by itself establish signaling by the intact receptor. Proposed replacements: BMP binding |
| GO:0005515 protein binding | IPI PMID:21543859 Purification, crystallization and preliminary data analysis ... | MODIFY | Summary: Engineered GDF5 R57A forms a ligand-binding complex with BMPR1A. Reason: PMID:21543859 prepares and crystallizes purified GDF5 R57A with the human BRIA extracellular domain. Refine P43026 protein binding to BMP binding while explicitly restricting the high-affinity result to this engineered ligand. It is not evidence of a natural BMPR1A isoform or identical affinity for wild-type GDF5. Proposed replacements: BMP binding Supporting Evidence: PMID:21543859 GDF5 variant R57A, which exhibits a high affinity in the subnanomolar range for BRIA |
| GO:0005515 protein binding | IPI PMID:21791611 TSC-22 promotes transforming growth factor Ξ²-mediated cardia... | KEEP AS NON CORE | Summary: TSC22D1 is a documented BMPR1A-associated regulator. Reason: The accessible PMID:21791611 abstract emphasizes TGF-beta receptor regulation, while the BMPR1A UniProt record explicitly cites this source for interaction with TSC22D1/TSC-22, matching Q15714. Retain the curated interaction as non-core with that target-specific corroboration; do not assign TSC22D1 transcriptional or adaptor activity to BMPR1A. Full target-assay details remain unread. |
| GO:0005515 protein binding | IPI PMID:21976273 New insights into the molecular mechanism of multiple synost... | UNDECIDED | Summary: The GDF5 interaction is plausible, but the experiment in this reference is not resolved. Reason: PMID:21976273 emphasizes GDF5 knuckle-epitope mutation, noggin resistance and type II receptor effects. The accessible abstract does not resolve the exact BMPR1AβP43026 experiment or ligand construct. Preserve this source-specific assertion pending full-text inspection rather than deny the independently established GDF5βBMPR1A interaction. |
| GO:0005515 protein binding | IPI PMID:21976273 New insights into the molecular mechanism of multiple synost... | UNDECIDED | Summary: The BMPR1AβBMPR2 association needs an assay-specific reading of PMID:21976273. Reason: The original Q13873 partner is preserved. Type I/type II receptors cooperate biologically, but the accessible GDF5/antagonist-centered abstract does not establish what direct interaction or co-complex assay supports this row. Do not infer physical contact merely from membership of a ligand-assembled receptor complex. |
| GO:0005515 protein binding | IPI PMID:24098149 A GDF5 point mutation strikes twice--causing BDA1 and SYNS2. | MODIFY | Summary: Wild-type GDF5 binds BMPR1A in the ligand-variant comparison. Reason: Selected Results and Methods of PMID:24098149 directly compare wild-type GDF5 and W414R binding to BMPR1A ectodomain. Refine the preserved P43026 interaction to BMP binding, without treating the mutant affinity or BMPR1B preference as absence of wild-type BMPR1A binding. Proposed replacements: BMP binding Supporting Evidence: PMID:24098149 Wild type GDF5 binds BMPR1A with a weaker affinity compared to BMPR1B |
| GO:0005515 protein binding | IPI PMID:24904118 HFE interacts with the BMP type I receptor ALK3 to regulate ... | KEEP AS NON CORE | Summary: HFE associates with BMPR1A and stabilizes receptor presentation at the cell surface. Reason: PMID:24904118 supports the Q30201 interaction and altered ALK3 degradation/trafficking. Retain this regulatory association as non-core; it neither makes BMPR1A a transferrin receptor nor proves a complete HFEβtransferrin-receptor assembly. No defensible specific replacement for this interaction is established. Supporting Evidence: PMID:24904118 HFE was found to associate with ALK3 |
| GO:0005515 protein binding | IPI PMID:25938661 Repulsive guidance molecule is a structural bridge between n... | MODIFY | Summary: Human BMPR1A ectodomain directly binds BMP2 in the RGM study. Reason: Selected Results and Methods of PMID:25938661 include SPR using purified human BMPR1A ectodomain and BMP2. Preserve P12643 and refine to BMP binding. RGM-mediated bridging and soluble-receptor ligand interception do not imply scaffold activity or endogenous endocytosis by BMPR1A. Proposed replacements: BMP binding Supporting Evidence: PMID:25938661 The secreted ectodomain of BMPR1A (eBMPR1A) bound to BMP2 with a Kd of 280Β±10 nM |
| GO:0005515 protein binding | IPI PMID:33308444 SCUBE3 loss-of-function causes a recognizable recessive deve... | KEEP AS NON CORE | Summary: SCUBE3 is a documented BMPR1A-associated BMP signaling regulator. Reason: PMID:33308444 and the target-specific UniProt interaction statement support association with Q8IX30. Retain it as non-core under the scoped generic-binding instruction. SCUBE3 co-receptor/scaffold biology must not be reassigned to BMPR1A; complete target-specific experimental details were not independently read. |
| GO:0005524 ATP binding | IDA PMID:12065756 SB-431542 is a potent and specific inhibitor of transforming... | ACCEPT | Summary: ATP binding is part of the BMPR1A kinase mechanism. Reason: Retain the PMID:12065756 experimental assertion with curator deference: activated human ALK3 is present in the indexed Methods, while the original ATP-binding assay was not independently retrieved. The ATP-dependent receptor catalytic mechanism is corroborated by UniProt and R-HSA-201476. This does not infer kinase inactivity from the inhibitor paper title. |
| GO:0005524 ATP binding | IEA GO_REF:0000120 | ACCEPT | Summary: BMPR1A uses ATP for receptor kinase catalysis. Reason: The integrated electronic ATP-binding annotation is consistent with the conserved intracellular kinase domain and ATP-dependent catalytic reactions recorded in UniProt. It describes a component of the same receptor mechanism, not a separate core function. |
| GO:0005886 plasma membrane | EXP PMID:19726563 The transforming growth factor-beta type III receptor mediat... | ACCEPT | Summary: BMPR1A signals from the plasma membrane and is retained there by TGFBR3. Reason: PMID:19726563 distinguishes TGFBR3-mediated ALK3 surface retention from beta-arrestin-linked ALK6 internalization. Retain the experimentally supported plasma-membrane location without transferring the ALK6 trafficking mechanism to BMPR1A. Supporting Evidence: PMID:19726563 cell surface retention of ALK3, independently of beta-arrestin2 |
| GO:0005886 plasma membrane | IBA GO_REF:0000033 | ACCEPT | Summary: Plasma-membrane localization is conserved for BMPR1A. Reason: The PAINT node-based inference agrees with receptor topology and direct ALK3 surface-trafficking evidence. No target-specific loss or relocation contradicts the ancestral localization; donor number is not a measure of IBA quality. |
| GO:0005886 plasma membrane | IDA PMID:15657086 Dynamics and interaction of caveolin-1 isoforms with BMP-rec... | ACCEPT | Summary: BMPR1A localizes to membrane domains that include caveolin-associated regions. Reason: The PMID:15657086 abstract directly describes BRIa distribution relative to caveolin domains. Retain plasma-membrane location; caveolin alpha/beta isoforms in that paper do not imply BMPR1A isoforms, and BRII-focused immunoprecipitation conclusions should not be transferred wholesale. Supporting Evidence: PMID:15657086 BRIa and BRII colocalize with caveolin-1 isoforms alpha and beta on the cell surface |
| GO:0005886 plasma membrane | IEA GO_REF:0000044 | ACCEPT | Summary: The UniProt cellular-location mapping correctly places BMPR1A at the plasma membrane. Reason: The source record identifies a single-pass cell-membrane receptor and cites experimental surface-trafficking evidence. This mapping describes the location where ligand recognition and receptor signaling occur. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201443 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: Type II receptor phosphorylation activates BMPR1A in a cell-surface receptor complex. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201453 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: The cached event title names BMP R-SMAD dissociation, but its body describes TGF-beta/SMAD2/3, a title/body mismatch. Retain the location based on independent ALK3 localization evidence; do not use the mismatched event prose as a BMP-specific assay. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201457 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: BMP2 engages the cell-surface receptor complex. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201475 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: I-SMAD competition regulates access to the membrane receptor kinase. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201476 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: The membrane-localized type I receptor phosphorylates R-SMAD1/5/8. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201648 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: Endofin recruitment places R-SMADs near the membrane-associated receptor. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-201821 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: I-SMAD/Smurf regulation acts on BMPR1A as receptor substrate, not as an E3 ligase. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-202604 | ACCEPT | Summary: The Reactome event places the BMPR1A signaling receptor at the plasma membrane. Reason: Both pre-existing and ligand-induced heteromeric receptor assemblies are compatible with plasma-membrane signaling. The location is consistent with direct ALK3 cell-surface studies. |
| GO:0005901 caveola | IMP PMID:15657086 Dynamics and interaction of caveolin-1 isoforms with BMP-rec... | KEEP AS NON CORE | Summary: BMPR1A can occupy caveolin-associated plasma-membrane domains. Reason: PMID:15657086 supports a caveolar distribution context for BRIa, which is narrower than its general cell-surface localization. Preserve this localization as non-core and condition-dependent; do not claim all receptors are permanently caveolar or transfer the paperβs BRII immunoprecipitation results to BRIa. |
| GO:0006955 immune response | IMP PMID:16886151 Association of polymorphisms of IGF1R and genes in the trans... | UNDECIDED | Summary: A BMPR1A polymorphism association does not resolve a direct immune-response role. Reason: PMID:16886151 reports candidate SNP associations with bacteremia in sickle-cell anemia. The accessible abstract does not identify the molecular or cellular immune-response step executed by BMPR1A or the full basis of the curated IMP row. Keep the source assertion pending fuller evidence; do not convert association into a defining immune function or claim the annotation is wrong. |
| GO:0007178 cell surface receptor protein serine/threonine kinase signaling pathway | IEA GO_REF:0000002 | ACCEPT | Summary: BMPR1A carries out cell-surface serine/threonine receptor signaling. Reason: The InterPro mapping matches the intrinsic receptor kinase architecture and the type II-to-type I-to-SMAD sequence of catalytic activation. BMP signaling is the more specific mechanistic instance already represented in the source rows. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IMP PMID:36641752 The Integrator complex desensitizes cellular response to TGF... | UNDECIDED | Summary: The human ALK3/Integrator arm supports BMP-superfamily signaling, but the specific TGF-beta pathway assertion needs clarification. Reason: PMID:36641752 includes human experiments; indexed primary discussion explicitly identifies engineered Alk3 QD. It is not a wrong-gene or Drosophila-only reference. The accessible material does not independently establish wild-type BMPR1A participation in a TGF-beta-ligand-specific pathway rather than BMP signaling. Preserve the experimental assertion while the precise pathway context is checked. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | TAS PMID:8397373 Activin receptor-like kinases: a novel subclass of cell-surf... | MARK AS OVER ANNOTATED | Summary: The ALK3 cloning evidence supports receptor-family membership, but not this specific TGF-beta pathway assignment. Reason: PMID:8397373 predicts TGF-beta-superfamily receptor membership from human ALK3 sequence and topology. That prediction is broader than GO:0007179, which specifies a TGF-beta receptor signaling pathway; BMP signaling has its own term, GO:0030509. Mark this TAS pathway attribution as over-specific relative to the evidence described in the accessible abstract. This is not evidence that BMPR1A cannot participate in TGF-beta cross-talk, nor a claim that the unread full text excludes it. Independently supported BMP signaling is already reviewed in its existing rows, so no replacement duplicate is added. |
| GO:0009897 external side of plasma membrane | IDA PMID:24904118 HFE interacts with the BMP type I receptor ALK3 to regulate ... | ACCEPT | Summary: BMPR1A presents its ligand-binding domain on the external side of the plasma membrane. Reason: PMID:24904118 reports increased cell-surface ALK3 accumulation following HFE association; the location is compatible with its extracellular ligand-binding domain and membrane topology. Retain the source annotation without equating cell-surface detection with demonstration of the complete HFEβtransferrin-receptor complex. |
| GO:0009953 dorsal/ventral pattern formation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: BMPR1A contributes to conserved BMP-dependent dorsalβventral patterning. Reason: The PAINT inference is a phylogenetic assertion about developmental signaling, not a pairwise donor transfer. This broad developmental output is consistent with BMP receptor biology but is not a separate defining molecular activity. No loss-of-function evidence specific to the human receptor contradicts the placement. |
| GO:0009986 cell surface | IEA GO_REF:0000120 | ACCEPT | Summary: BMPR1A is exposed at the cell surface. Reason: The source mapping/orthology assertion agrees with human ALK3 surface trafficking in PMID:19726563 and HFE-dependent surface accumulation in PMID:24904118. Cell-surface receptor presentation is part of the ligand-recognition mechanism. |
| GO:0009986 cell surface | ISS GO_REF:0000024 | ACCEPT | Summary: BMPR1A is exposed at the cell surface. Reason: The source mapping/orthology assertion agrees with human ALK3 surface trafficking in PMID:19726563 and HFE-dependent surface accumulation in PMID:24904118. Cell-surface receptor presentation is part of the ligand-recognition mechanism. |
| GO:0010628 positive regulation of gene expression | IMP PMID:24882581 MicroRNA-885-3p inhibits the growth of HT-29 colon cancer ce... | KEEP AS NON CORE | Summary: BMPR1A-dependent signaling increases downstream gene expression in the HT-29 model. Reason: PMID:24882581 links BMPR1A/BMP/SMAD signaling with ID1 expression and tumor phenotypes. Retain the positive-regulation assertion as a downstream cellular outcome; BMPR1A does not itself bind DNA or act as a transcription factor. |
| GO:0010629 negative regulation of gene expression | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: The mouse orthology assertion records a context in which BMPR1A signaling reduces gene expression. Reason: GO_REF:0000024 transfers a curated mouse P36895 outcome. Positive and negative transcriptional consequences can differ by target gene, cell type and signaling context; they are not contradictory molecular activities. Retain the source-level consequence as non-core without inventing an unread target-gene assay. |
| GO:0010665 regulation of cardiac muscle cell apoptotic process | ISS NOT GO_REF:0000024 | KEEP AS NON CORE | Summary: The NOT assertion is retained as a bounded mouse developmental observation, not universal absence of an apoptosis role. Reason: The source is an ISS transfer from mouse P36895. PMID:18667463 provides compatible SM22alpha-Cre E10.5βE11 evidence of reduced myocardial proliferation without enhanced TUNEL staining, while contrasting later deletion contexts with increased apoptosis. Preserve negation and restrict interpretation to the observed developmental setting; this paper is corroboration, not a verified reconstruction of the original donor chain. |
| GO:0014912 negative regulation of smooth muscle cell migration | IMP PMID:18667463 SM22alpha-targeted deletion of bone morphogenetic protein re... | KEEP AS NON CORE | Summary: BMPR1A restrains basal smooth-muscle migration while enabling a stimulated migratory response. Reason: Selected Methods and Results of PMID:18667463 show increased basal migration after BMPR1A knockdown in human pulmonary-artery smooth-muscle cells, but loss of PDGF-BB-directed migration after serum starvation. The negative-regulation term is defensible for the basal condition. Retain it as context-specific and do not reverse its direction from the abstract alone. Supporting Evidence: PMID:18667463 basal levels of migration were increased in SiBmpr1a transfected HPASMC |
| GO:0016020 membrane | IEA GO_REF:0000002 | ACCEPT | Summary: BMPR1A is an integral membrane receptor. Reason: The InterPro membrane assertion fits the experimentally supported plasma-membrane receptor and single transmembrane helix. Retain the broad correct location alongside more precise surface annotations. |
| GO:0016020 membrane | TAS PMID:8397373 Activin receptor-like kinases: a novel subclass of cell-surf... | ACCEPT | Summary: Human ALK3 has the architecture of a single-pass membrane receptor. Reason: PMID:8397373 describes the human 532-residue clone and its hydrophobic transmembrane segment. The source supports membrane topology; subsequent ALK3 localization studies establish cell-surface presentation. |
| GO:0030154 cell differentiation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: BMPR1A mediates conserved BMP-dependent differentiation responses. Reason: The PAINT inference is consistent with receptor signaling in several lineages, including human mesenchymal-cell differentiation in PMID:18436533. Retain this broad developmental process as non-core rather than identify it with a single tissue-specific phenotype. |
| GO:0030425 dendrite | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: A rat orthology transfer places BMPR1A in dendrites. Reason: The GO_REF:0000107 sources are rat Q78EA7/ENSRNOP00000074885, not mouse. Preserve this neuronal-location assertion as non-core; it is not a direct human localization measurement, and soluble BMPR1A-Fc inhibition of BMP5 in PMID:11580864 does not independently prove endogenous dendritic receptor localization. |
| GO:0030501 positive regulation of bone mineralization | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Electronic evidence links BMPR1A signaling to bone mineralization. Reason: The ARBA assertion is consistent with the osteogenic BMP response, but mineralization is a tissue-level outcome of receptor signaling. Retain it as non-core without treating a ligand-induced mineralization assay as a direct biochemical activity of BMPR1A. |
| GO:0030501 positive regulation of bone mineralization | IMP PMID:18436533 BMP-2/4 and BMP-6/7 differentially utilize cell surface rece... | KEEP AS NON CORE | Summary: BMPR1A contributes to osteogenic responses in human mesenchymal cells. Reason: PMID:18436533 separates BMP-induced mineralization from receptor RNAi and osteoblast-marker analyses. Preserve the curated IMP mineralization assertion, while limiting the independently read evidence to the receptor perturbation and differentiation context rather than claiming a receptor-specific mineralization assay was verified. |
| GO:0030509 BMP signaling pathway | IBA GO_REF:0000033 | ACCEPT | Summary: BMPR1A is a conserved signaling receptor in the BMP pathway. Reason: The PAINT node-based inference agrees with direct ligand/receptor and downstream SMAD evidence. The receptor is an active catalytic signaling component, not simply a downstream substrate or marker; there is no target-specific evidence of functional loss. |
| GO:0030509 BMP signaling pathway | IDA PMID:12065756 SB-431542 is a potent and specific inhibitor of transforming... | ACCEPT | Summary: Activated human ALK3 participates in BMP signaling. Reason: PMID:12065756 includes BMP-receptor comparators and activated human ALK3 in the indexed Methods. Retain the source annotation with curator deference and the independently established receptor mechanism; do not claim the inaccessible complete assays were reread. |
| GO:0030509 BMP signaling pathway | IDA PMID:18436533 BMP-2/4 and BMP-6/7 differentially utilize cell surface rece... | ACCEPT | Summary: Human BMPR1A transduces BMP signals in receptor perturbation experiments. Reason: PMID:18436533 demonstrates preferential utilization of BMPR1A by BMP2/4 in human bone-marrow mesenchymal cells. Receptor dependence varies with ligand and cell context; the study does not make BMPR1A the sole receptor for all BMPs. Supporting Evidence: PMID:18436533 BMPR1A is utilized principally by BMP-2/4 and only minimally by BMP-6/7 |
| GO:0030509 BMP signaling pathway | IDA PMID:24904118 HFE interacts with the BMP type I receptor ALK3 to regulate ... | ACCEPT | Summary: HFE regulates BMP output by associating with the ALK3/BMPR1A receptor. Reason: PMID:24904118 links receptor stabilization and surface accumulation to increased BMP/SMAD/hepcidin output. BMPR1A contributes the receptor signaling mechanism; this does not assign HFE iron sensing or receptor ubiquitination machinery to BMPR1A. |
| GO:0030509 BMP signaling pathway | IDA PMID:9389648 Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-indu... | ACCEPT | Summary: Activated BMPR1A drives the BMP/SMAD arm examined in the SMAD4 study. Reason: Selected canonical Methods of PMID:9389648 explicitly use BMPR-IA(Q233D) with BMP4 stimulation. Retain BMP signaling; the experimental receptor is an activated construct and the paperβs nuclear transcriptional functions belong to SMAD complexes, not BMPR1A itself. Supporting Evidence: PMID:9389648 BMPR-IA(Q233D) |
| GO:0030509 BMP signaling pathway | IMP PMID:24882581 MicroRNA-885-3p inhibits the growth of HT-29 colon cancer ce... | ACCEPT | Summary: BMPR1A supports BMP/SMAD pathway activity in the HT-29 perturbation study. Reason: PMID:24882581 targets BMPR1A and measures downstream pathway changes. This supports the same receptor signaling mechanism despite the tumor-specific experimental setting; angiogenesis is treated separately as a non-core consequence. |
| GO:0030509 BMP signaling pathway | ISS GO_REF:0000024 | ACCEPT | Summary: Mouse BMPR1A signaling evidence transfers consistently to the human BMP receptor. Reason: The curator orthology transfer agrees with conserved receptor architecture and direct human ligand/signaling experiments. Retain the BMP pathway assertion without presenting the donor study as an experiment on human developmental tissues. |
| GO:0030509 BMP signaling pathway | TAS Reactome:R-HSA-201451 | ACCEPT | Summary: BMPR1A is part of the curated BMP receptor-to-SMAD signaling pathway. Reason: R-HSA-201451 describes BMP signal transduction through type I/type II receptor complexes. BMPR1A performs the activated type I receptor kinase step, supporting direct pathway participation. |
| GO:0032915 positive regulation of transforming growth factor beta2 production | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse evidence links BMPR1A signaling to increased TGF-beta2 production. Reason: The curated ISS transfer from P36895 records an indirect signaling output. Retain it as non-core without treating production of another ligand as TGF-beta2 receptor recognition by BMPR1A or inventing a direct transcriptional mechanism. |
| GO:0035912 dorsal aorta morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports dorsal-aorta morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for embryonic dorsal-aortic development. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0035912 dorsal aorta morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports dorsal-aorta morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for embryonic dorsal-aortic development. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0036122 BMP binding | IEA GO_REF:0000120 | ACCEPT | Summary: BMP binding is an intrinsic part of BMPR1A ligand recognition. Reason: The integrated mapping agrees with directly observed BMP2 ectodomain complexes and biochemical ligand binding. This activity belongs to the receptor, whereas BMP receptor binding describes the reciprocal activity of the ligand. |
| GO:0036122 BMP binding | IPI PMID:18184661 Bone morphogenetic proteins signal through the transforming ... | ACCEPT | Summary: The curated BMP2-binding assertion is consistent with established BMPR1A ligand recognition. Reason: PMID:18184661 focuses on the type III receptor, but that title does not exclude type I receptor comparator experiments. Retain P12643 BMP binding with curator deference and independent direct BMPR1A/BMP2 structures; the complete original comparator assay was not independently read. |
| GO:0042803 protein homodimerization activity | IDA PMID:18436533 BMP-2/4 and BMP-6/7 differentially utilize cell surface rece... | KEEP AS NON CORE | Summary: BMPR1A self-associates in full-length receptor BRET experiments. Reason: PMID:18436533 uses human receptor constructs and saturation/competition BRET measurements, supporting BMPR1A self-association. Retain this receptor-assembly component as non-core rather than infer a purified direct interface, fixed physiological stoichiometry or an activity independent of receptor signaling. |
| GO:0043025 neuronal cell body | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: A rat orthology transfer places BMPR1A in neuronal cell bodies. Reason: The source donor is rat Q78EA7/ENSRNOP00000074885, not mouse. Retain this specialized cellular-location annotation as non-core, preserving the distinction between an inferred neuronal compartment and directly demonstrated general cell-surface receptor localization. |
| GO:0043235 signaling receptor complex | IBA GO_REF:0000033 | ACCEPT | Summary: BMPR1A operates within a signaling receptor complex. Reason: The PAINT complex assertion matches ligand/type I/type II assembly and the curated Reactome receptor events. The complexes can assemble before or after ligand binding; an exact constitutive stoichiometry or direct ectodomainβectodomain contact is not implied. |
| GO:0045669 positive regulation of osteoblast differentiation | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Electronic inference links BMPR1A to promotion of osteoblast differentiation. Reason: The ARBA annotation is compatible with human mesenchymal-cell signaling and receptor perturbations in PMID:18436533. Retain the lineage-specific outcome as non-core, distinct from the intrinsic receptor kinase activity. |
| GO:0045669 positive regulation of osteoblast differentiation | IMP PMID:18436533 BMP-2/4 and BMP-6/7 differentially utilize cell surface rece... | KEEP AS NON CORE | Summary: BMPR1A promotes osteoblastic differentiation responses in human mesenchymal cells. Reason: PMID:18436533 uses receptor knockdown and osteoblast differentiation markers, with BMP2/4 preferentially using BMPR1A in this cell system. Retain the process in that ligand/cell context rather than declare a universal receptor requirement for all osteogenic BMP ligands. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: BMPR1A signaling can promote RNA polymerase II-dependent gene expression. Reason: GO:0045944 describes positive regulation of Pol II transcription, not transcription itself. BMPR1A activates R-SMAD effectors that regulate transcription, and ALK3-dependent promoter responses in PMID:18326817 corroborate this broad ARBA inference. Retain the regulatory outcome as non-core; this does not assign DNA binding or polymerase catalysis to the receptor. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IMP PMID:18326817 Hemojuvelin regulates hepcidin expression via a selective su... | KEEP AS NON CORE | Summary: ALK3-dependent BMP signaling promotes hepcidin-promoter and reporter output. Reason: Selected full-text Methods and Results of PMID:18326817 describe ALK3 RNAi reducing BMP/HJV-dependent reporter and hepcidin-promoter output in Hep3B/Huh-7 cells. The receptor kinase contributes to the signaling process that activates transcription through SMAD effectors. Retain this experimentally supported regulatory outcome as non-core. Involvement in regulation of transcription does not imply participation in RNA synthesis or direct promoter binding. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse orthology supports transcriptional activation downstream of BMPR1A. Reason: The mouse P36895 orthology transfer is consistent with conserved receptor activation of SMAD-dependent transcriptional regulation. GO:0045944 describes that regulatory process, not Pol II catalysis. Retain the curated inference as non-core without inventing a donor promoter assay or claiming direct DNA binding; PMID:9389648 supplies receptor-to-SMAD transcriptional context. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | ISS PMID:18667463 SM22alpha-targeted deletion of bone morphogenetic protein re... | KEEP AS NON CORE | Summary: The mouse source connects Bmpr1a signaling to transcriptional output. Reason: PMID:18667463 reports reduced Mmp2/Mmp9 expression following Bmpr1a loss, including mouse developmental and human vascular-cell experiments. Preserve this row as an ISS transfer from mouse P36895, retaining the curator-supported transcriptional regulatory outcome as non-core. Expression endpoints alone do not isolate transcription from RNA stability, and this row is not relabeled as direct human transcriptional-mechanism evidence. |
| GO:0046332 SMAD binding | IDA PMID:12065756 SB-431542 is a potent and specific inhibitor of transforming... | ACCEPT | Summary: SMAD engagement is part of BMPR1A receptor kinase signaling. Reason: Retain the PMID:12065756 IDA assertion with curator deference; activated human ALK3 appears in indexed Methods, but the original SMAD-association experiment was not independently read. Direct BMP type I receptor phosphorylation of SMAD1 and R-HSA-201476 support the same receptorβsubstrate mechanism. |
| GO:0046332 SMAD binding | IEA GO_REF:0000117 | ACCEPT | Summary: BMPR1A engages SMAD substrates during receptor signaling. Reason: The electronic SMAD-binding annotation is consistent with the catalytic receptor-to-R-SMAD interaction. It is not evidence that BMPR1A has the nuclear transcriptional activities of the SMAD partners. |
| GO:0048568 embryonic organ development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse orthology supports a broad role in embryonic organ development. Reason: Retain the curated P36895 transfer as a pleiotropic developmental consequence of BMP receptor signaling. PMID:18667463 provides a compatible cardiac/vascular example, not proof that the original donor assay or every organ phenotype has been independently reconstructed. |
| GO:0048863 stem cell differentiation | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: The curated mouse-source annotation links BMPR1A signaling to stem-cell differentiation. Reason: The original MGI:1338938 supporting entity is preserved without inventing a source symbol or assay. This broad differentiation output is compatible with BMP receptor signaling and is retained as non-core; the specific donor experiment was not independently reconstructed. |
| GO:0060043 regulation of cardiac muscle cell proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports regulation of cardiac myocyte proliferation downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for control of cardiac myocyte proliferation. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0060043 regulation of cardiac muscle cell proliferation | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports regulation of cardiac myocyte proliferation downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for control of cardiac myocyte proliferation. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0060045 positive regulation of cardiac muscle cell proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports positive regulation of cardiac myocyte proliferation downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for promotion of cardiac myocyte proliferation. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0060045 positive regulation of cardiac muscle cell proliferation | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports positive regulation of cardiac myocyte proliferation downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for promotion of cardiac myocyte proliferation. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:24904118 HFE interacts with the BMP type I receptor ALK3 to regulate ... | ACCEPT | Summary: ALK3 stabilization by HFE increases downstream SMAD1/5/8 signaling. Reason: PMID:24904118 links HFEβALK3 association and surface receptor abundance to BMP/SMAD output. Retain the positive SMAD-signaling assertion as part of the receptor mechanism, without inferring a complete HFEβtransferrin-receptor assembly. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:9389648 Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-indu... | ACCEPT | Summary: Activated BMPR1A supports the SMAD1 signaling arm. Reason: PMID:9389648 uses activated BMPR-IA(Q233D) and BMP4 in the canonical Methods, separating receptor activation from SMAD4-dependent transcriptional functions. Retain positive SMAD signaling while respecting the engineered receptor and assay context. Supporting Evidence: PMID:9389648 activated BMP type I receptor |
| GO:0060391 positive regulation of SMAD protein signal transduction | IMP PMID:24882581 MicroRNA-885-3p inhibits the growth of HT-29 colon cancer ce... | ACCEPT | Summary: BMPR1A perturbation alters downstream SMAD signaling in HT-29 cells. Reason: PMID:24882581 links reduced BMPR1A to reduced BMP/SMAD/ID1 signaling. The mechanistic receptor-to-SMAD role is core even though the experimental tumor/angiogenesis consequences are context-specific. |
| GO:0060412 ventricular septum morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports ventricular-septum morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for formation of the ventricular septum. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0060412 ventricular septum morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports ventricular-septum morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for formation of the ventricular septum. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0060928 atrioventricular node cell development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports atrioventricular-node cell development downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for development of specialized atrioventricular conduction cells. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0060928 atrioventricular node cell development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports atrioventricular-node cell development downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for development of specialized atrioventricular conduction cells. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0061626 pharyngeal arch artery morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports pharyngeal-arch artery morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for development of the pharyngeal arch arteries. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0061626 pharyngeal arch artery morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports pharyngeal-arch artery morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for development of the pharyngeal arch arteries. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:0071363 cellular response to growth factor stimulus | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: BMPR1A mediates a conserved cellular response to extracellular growth factors. Reason: The PAINT process assertion is biologically consistent with BMP ligand reception, but this broad response term adds no separate defining mechanism beyond BMP receptor signaling. Retain it as non-core without challenging ancestral placement on donor-count grounds. |
| GO:0071773 cellular response to BMP stimulus | IMP PMID:18326817 Hemojuvelin regulates hepcidin expression via a selective su... | ACCEPT | Summary: ALK3/BMPR1A participates in cellular responses to BMP ligands. Reason: PMID:18326817 examines HJV-supported BMP signaling, with selected archived full text supporting ALK3-dependent reporter responses in hepatoma-cell contexts. This is compatible with the receptor mechanism; receptor preference remains ligand- and cell-dependent. Supporting Evidence: PMID:18326817 HJV can use all 3 BMP type I receptors (ALK2, ALK3, and ALK6) in vitro |
| GO:0098821 BMP receptor activity | IDA PMID:12065756 SB-431542 is a potent and specific inhibitor of transforming... | ACCEPT | Summary: BMPR1A has BMP receptor activity. Reason: The PMID:12065756 annotation is consistent with the human ALK3 construct identified in indexed Methods and independent ligand-binding/signaling studies. Retain the experimental assertion with curator deference despite incomplete access to the original full assays; it defines the ligand-coupled receptor kinase mechanism. |
| GO:0098821 BMP receptor activity | IEA GO_REF:0000120 | ACCEPT | Summary: The integrated annotation correctly identifies BMPR1A as a BMP receptor. Reason: Extracellular BMP recognition coupled to a transmembrane serine/threonine kinase and SMAD signaling is the defining activity of human P36894. This is more specific for core synthesis than the broad historical TGF-beta-superfamily type I designation. |
| GO:0098821 BMP receptor activity | ISS GO_REF:0000024 | ACCEPT | Summary: The mouse-to-human receptor-activity transfer agrees with direct human BMPR1A evidence. Reason: The curated P36895 orthology assertion is supported independently by human receptor ligand-binding and signaling studies. Retain BMP receptor activity without implying every mouse developmental phenotype has been measured in humans. |
| GO:1900006 positive regulation of dendrite development | TAS PMID:11580864 Bone morphogenetic protein-5 (BMP-5) promotes dendritic grow... | UNDECIDED | Summary: Soluble BMPR1A-Fc inhibits BMP5-driven dendrites, but endogenous receptor-specific participation remains unresolved. Reason: PMID:11580864 uses a soluble receptor ectodomain as a ligand trap in cultured sympathetic neurons; selected primary text explicitly leaves endogenous neuronal receptor binding open. The corresponding GO-CAM is curator evidence for a BMP5 dendrite-growth context, not an additional endogenous-receptor experiment. Keep the TAS assertion pending clarification of receptor-specific evidence; do not treat ligand interception as a BMPR1A knockout. |
| GO:1902895 positive regulation of miRNA transcription | IEA GO_REF:0000107 | UNDECIDED | Summary: The specific mouse-to-human miRNA-transcription transfer remains unresolved. Reason: The GO_REF:0000107 transfer names mouse P36895 and ENSMUSP00000035900, but the original donor experiment could not be recovered in the targeted source check. General BMP/SMAD-dependent gene induction does not establish this particular miRNA-transcription claim or distinguish transcription from miRNA processing. Preserve the source assertion pending donor evidence; the absence of receptor DNA binding is not the basis for doubt. |
| GO:1904414 positive regulation of cardiac ventricle development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports promotion of cardiac ventricle development downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for growth and development of the cardiac ventricles. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:1904414 positive regulation of cardiac ventricle development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports promotion of cardiac ventricle development downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for growth and development of the cardiac ventricles. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. PMID:18667463 provides compatible mouse SM22alpha-Cre evidence for reduced myocardial proliferation and ventricular-wall abnormalities, without identifying it as the original donor experiment. |
| GO:1904707 positive regulation of vascular associated smooth muscle cell proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Orthology supports promotion of vascular smooth-muscle proliferation by BMPR1A. Reason: The mouse-derived GO_REF:0000107 transfer is consistent with human pulmonary smooth-muscle perturbations in PMID:18667463. Preserve the donor provenance and retain the proliferation outcome as non-core rather than merge it with the distinct basal/stimulated migration effects. |
| GO:1904707 positive regulation of vascular associated smooth muscle cell proliferation | IMP PMID:18667463 SM22alpha-targeted deletion of bone morphogenetic protein re... | KEEP AS NON CORE | Summary: BMPR1A supports growth of human pulmonary-artery smooth-muscle cells. Reason: PMID:18667463 includes human-cell RNAi, proliferation assays and cell counts alongside mouse developmental experiments. Retain the positive proliferation assertion in that cellular context; it is separate from the paperβs condition-dependent effects on migration. |
| GO:1905285 fibrous ring of heart morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports cardiac fibrous-ring morphogenesis downstream of BMPR1A signaling. Reason: Retain the automated Ensembl orthology assertion from mouse P36895 for formation of the fibrous support at the atrioventricular junction. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:1905285 fibrous ring of heart morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: Mouse-derived evidence supports cardiac fibrous-ring morphogenesis downstream of BMPR1A signaling. Reason: Retain the curator-reviewed orthology assertion from mouse P36895 for formation of the fibrous support at the atrioventricular junction. This is a plausible conserved developmental use of BMPR1A signaling, not a separate molecular activity. The exact donor assay was not independently reconstructed; the source transfer is preserved rather than presented as a human developmental experiment. |
| GO:1905292 regulation of neural crest cell differentiation | ISS NOT GO_REF:0000024 | UNDECIDED | Summary: The neural-crest NOT assertion requires an exact donor-source and timing reconciliation. Reason: Preserve the source ISS transfer from mouse P36895 and its negation. Early versus later conditional deletion studies can distinguish initial neural-crest differentiation from subsequent cardiac/neural-crest requirements, but the exact original donor evidence chain has not been verified. Do not infer a universal absence of BMPR1A involvement or remove negation from a positive phenotype in another Cre/stage context. |
| GO:1990262 anti-Mullerian hormone receptor signaling pathway | IDA PMID:12368913 Requirement of Bmpr1a for MΓΌllerian duct regression during m... | KEEP AS NON CORE | Summary: Bmpr1a functions as a type I receptor in AMH-dependent MΓΌllerian-duct regression. Reason: PMID:12368913 uses conditional mouse deletion in duct-associated mesenchyme and identifies Bmpr1a as part of the AMH pathway. Preserve the original IDA evidence code, but describe the actual genetic/developmental evidence rather than claim a human purified AMH-binding assay. This developmental use of the shared receptor machinery is retained as non-core. |
| GO:1990262 anti-Mullerian hormone receptor signaling pathway | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Mouse orthology supports BMPR1A participation in the AMH receptor pathway. Reason: GO_REF:0000107 transfers the conserved type I receptor role; PMID:12368913 provides compatible mouse mesenchymal genetics. Retain the pathway context without replacing BMPR1Aβs principal BMP receptor core or inferring that all AMH signaling uses it exclusively. |
| GO:1990712 HFE-transferrin receptor complex | IC PMID:24904118 HFE interacts with the BMP type I receptor ALK3 to regulate ... | UNDECIDED | Summary: Pairwise HFEβALK3 association does not yet resolve membership in the complete HFEβtransferrin-receptor complex. Reason: GO:1990712 requires HFE with a transferrin receptor. PMID:24904118 directly supports HFEβALK3 association, while indexed primary discussion describes weak TFR2 interaction and a possible HFE/TFR2/HJV/ALK3 assembly. The supplemental figure was not independently inspected. Preserve the IC assertion and its GO:0005515 support, but leave complete assembly uncertain rather than equate pairwise binding with a demonstrated complex. |
| GO:1990712 HFE-transferrin receptor complex | IEA GO_REF:0000117 | UNDECIDED | Summary: The electronic HFEβtransferrin-receptor complex assignment inherits unresolved assembly specificity. Reason: ARBA:ARBA00088952 supplies this source assertion. The HFEβALK3 association in PMID:24904118 supports a regulatory interaction but does not independently establish the full transferrin-receptor-containing assembly required by GO:1990712. Preserve the mapping pending assembly-specific evidence; this is not evidence that the interaction or complex is absent. |
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Download this section (compressed HTML)Q: How should the GO:0005025 ligand-specific definition be reconciled with its repeated use for BMPR1A in curated BMP and AMH GO-CAM activities?
Q: What assembly-specific evidence establishes simultaneous ALK3, HFE and a transferrin receptor in the GO:1990712 complex, beyond pairwise interactions and the proposed multicomponent model?
Q: Which exact donor experiments and conditional-deletion stages support the two negated developmental source assertions?
Q: Does PMID:11580864 or subsequent source evidence distinguish an endogenous neuronal BMPR1A requirement from inhibition by a soluble BMP-binding receptor trap?
Q: What direct BMPR1A immune-response mechanism, if any, supports the bacteremia-associated annotation from PMID:16886151?
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