TGFB1 encodes transforming growth factor beta-1, a secreted multifunctional cytokine of the TGF-beta superfamily. It is made as a proprotein cleaved in the Golgi into the latency-associated peptide (LAP) and the mature TGF-beta-1 chain, which stay associated as a latent complex stored in the extracellular matrix and tethered at the cell surface by LTBP, GARP (LRRC32) and NRROS (LRRC33); integrin-mediated force releases the active cytokine. Active TGF-beta-1 binds type I, II and III TGF-beta receptors to activate receptor serine/threonine kinase and SMAD signaling, controlling cell growth and differentiation, extracellular-matrix production and fibrosis, immune tolerance (regulatory T cells, IgA class switching), epithelial-to-mesenchymal transition, wound healing and many developmental processes.
| GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0001501 skeletal system development | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: skeletal system development. Reason: skeletal system development is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001558 regulation of cell growth | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: regulation of cell growth. Reason: regulation of cell growth is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001570 vasculogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: vasculogenesis. Reason: vasculogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001570 vasculogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: vasculogenesis. Reason: vasculogenesis is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0001657 ureteric bud development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: ureteric bud development. Reason: ureteric bud development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001666 response to hypoxia | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: response to hypoxia. Reason: response to hypoxia is an electronic (IEA) annotation under GO_REF:0000120. this term records that TGF-beta-1 expression or activity is modulated in the context of hypoxia; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001763 morphogenesis of a branching structure | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: morphogenesis of a branching structure. Reason: morphogenesis of a branching structure is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001837 epithelial to mesenchymal transition | IDA PMID:25893292 Syntenin regulates TGF-Ξ²1-induced Smad activation and the ep... | KEEP AS NON CORE | Summary: epithelial to mesenchymal transition. Reason: GO:0001837 epithelial to mesenchymal transition is supported by TGF-beta-1-mediated Smad activation driving EMT in A549 cells (E-cadherin repression, vimentin/Snail/Slug induction), modulated by syntenin's control of TbetaRI internalization. EMT is the canonical downstream SMAD-dependent program of the pathway, a consequence of the core receptor-binding function, so it is non-core. Supporting Evidence: PMID:25893292 transforming growth factor (TGF)-Ξ²1-mediated Smad activation and the epithelial-to-mesenchymal transition |
| GO:0001837 epithelial to mesenchymal transition | IDA PMID:28373289 miR-202 Diminishes TGFΞ² Receptors and Attenuates TGFΞ²1-Induc... | KEEP AS NON CORE | Summary: epithelial to mesenchymal transition. Reason: GO:0001837 epithelial to mesenchymal transition. In pancreatic cancer cells TGF-beta-1 is the secreted ligand whose binding to TGFBR2/TGFBR1 initiates SMAD2/3 signaling that drives the EMT program; this paper uses exogenous TGF-beta-1 as the canonical EMT inducer and shows miR-202-mediated knockdown of the receptors blocks that response. EMT itself is a downstream transcriptional/morphological program executed by Snail/ZEB/Twist transcription factors acting downstream of receptor engagement, not a molecular activity TGF-beta-1 performs; the gene product's role is restricted to the upstream ligand/receptor-binding step. Non-core because EMT is a context-specific (tumor) consequence of the core receptor-binding + SMAD signaling function rather than that function itself. Supporting Evidence: PMID:28373289 Transforming Growth Factor-beta 1 (TGF-Ξ²1) is a multifunctional cytokine secreted into the tumor microenvironment which primarily promotes the EMT process |
| GO:0001837 epithelial to mesenchymal transition | IDA PMID:29529050 Transmembrane protease, serine 4 (TMPRSS4) is upregulated in... | KEEP AS NON CORE | Summary: epithelial to mesenchymal transition. Reason: GO:0001837 epithelial to mesenchymal transition. In this study TGF-Ξ²1 (5 ng/mL) was applied to A549 alveolar epithelial cells as the positive control for EMT, where it strongly downregulated E-cadherin and raised Ξ±-SMA, i.e. drove the epithelial-to-mesenchymal phenotypic switch (the paper's own focus is TMPRSS4, which partially opposes this). EMT is a multi-gene transcriptional and phenotypic program executed downstream of TGFB1 receptor binding and SMAD signaling in the target epithelial cell, not a molecular activity the secreted ligand itself performs, so it is a non-core consequence of TGFB1's core receptor-binding/SMAD-initiating role. Supporting Evidence: PMID:29529050 Since the activation of TGF-Ξ² signaling causes epithelial to mesenchymal transition (EMT), a process that include the downregulation of the expression of E-cadherin |
| GO:0001837 epithelial to mesenchymal transition | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: epithelial to mesenchymal transition. Reason: epithelial to mesenchymal transition is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a principal inducer of EMT, but this is a multi-step cellular program executed by many downstream effectors; for the ligand it is a major downstream consequence of receptor binding and SMAD signaling rather than a core molecular activity. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001843 neural tube closure | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: neural tube closure. Reason: neural tube closure is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0001843 neural tube closure | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: neural tube closure. Reason: neural tube closure is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0002040 sprouting angiogenesis | IMP PMID:31368162 HIF1A/miR-20a-5p/TGFΞ²1 axis modulates adipose-derived stem c... | KEEP AS NON CORE | Summary: sprouting angiogenesis. Reason: GO:0002040 sprouting angiogenesis reflects TGF-beta-1 secreted by adipose-derived stem cells acting in a paracrine manner to promote angiogenesis of dermal microvascular endothelial cells; silencing TGFB1 reverses this angiogenic effect. Angiogenesis here is a paracrine, cell-non-autonomous outcome of the ligand reaching endothelial receptors, a downstream consequence of the core receptor-binding function, hence non-core. The abstract supports an angiogenesis role but does not specify the sprouting subtype, which rests on the uncited full text. Supporting Evidence: PMID:31368162 TGFB1-silenced ADSCs medium significantly reverses HDMECs angiogenesis |
| GO:0002062 chondrocyte differentiation | IDA PMID:15040835 Cooperation between TGF-beta and Wnt pathways during chondro... | KEEP AS NON CORE | Summary: chondrocyte differentiation. Reason: GO:0002062 chondrocyte differentiation records TGF-beta1 driving chondrogenic differentiation of human marrow stromal cells (induction of aggrecan and collagen type II). This is a lineage-specification outcome downstream of TGF-beta1/SMAD signaling (here acting synergistically with Wnt/beta-catenin), a tissue-specific developmental role rather than the core receptor-binding activity, so it is correctly non-core. Supporting Evidence: PMID:15040835 TGF-beta stimulated chondrocyte differentiation and inhibited adipocyte differentiation of hMSCs in vitro |
| GO:0002244 hematopoietic progenitor cell differentiation | IDA PMID:15451575 FLRG, member of the follistatin family, a new player in hema... | KEEP AS NON CORE | Summary: hematopoietic progenitor cell differentiation. Reason: GO:0002244 hematopoietic progenitor cell differentiation places TGF-beta-1 as a TGF-beta superfamily regulator of hematopoietic/erythroid progenitor fate, a downstream differentiation program driven through receptor/SMAD signaling and therefore non-core. The cached abstract concerns FLRG/follistatin and the activin/BMP control of erythropoiesis and does not mention TGF-beta-1 specifically, so the TGF-beta-1 attribution for this term rests on the uncited full text; it is retained rather than removed per the policy on experimental annotations whose full text is unavailable. |
| GO:0002248 connective tissue replacement involved in inflammatory response wound healing | TAS PMID:9639571 Thrombin stimulates fibroblast procollagen production via pr... | KEEP AS NON CORE | Summary: connective tissue replacement involved in inflammatory response wound healing. Reason: Annotates TGF-beta-1 to connective tissue replacement during inflammatory wound healing (TAS). This tissue-level fibrotic/repair process reflects TGF-beta-1-driven fibroblast activation and collagen matrix deposition, a downstream physiological consequence of receptor/SMAD signaling rather than the ligand's molecular activity, hence non-core. The cited abstract concerns thrombin-stimulated fibroblast procollagen production via PAR-1 and does not itself mention TGF-beta-1, so the TGF-beta-1-specific support rests on the uncached full text and no verbatim quote is asserted. |
| GO:0002460 adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily domains | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily domains. Reason: adaptive immune response based on somatic recombination of immune receptors built from immunoglobulin superfamily domains is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0002859 negative regulation of natural killer cell mediated cytotoxicity directed against tumor cell target | IDA PMID:24586048 TGF-Ξ²-inducible microRNA-183 silences tumor-associated natur... | KEEP AS NON CORE | Summary: negative regulation of natural killer cell mediated cytotoxicity directed against tumor cell target. Reason: GO:0002859 negative regulation of natural killer cell mediated cytotoxicity directed against tumor cell target. This is the central finding of the paper: TGF-Ξ²1-treated human NK cells show reduced tumor cytolysis and abrogated perforin polarization, because TGF-Ξ²1 induces miR-183 that represses the NK signaling adaptor DAP12. The suppression of NK anti-tumor killing is an indirect, cell-context-specific downstream consequence of TGFB1 receptor binding and SMAD signaling (operating through an induced microRNA), not a core molecular activity the ligand itself carries out, hence non-core. Supporting Evidence: PMID:24586048 TGF-Ξ²βtreated human NK cells exhibit reduced tumor cytolysis and abrogated perforin polarization to the immune synapse |
| GO:0003179 heart valve morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: heart valve morphogenesis. Reason: heart valve morphogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0003179 heart valve morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: heart valve morphogenesis. Reason: heart valve morphogenesis is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0003180 aortic valve morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: aortic valve morphogenesis. Reason: aortic valve morphogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0003180 aortic valve morphogenesis | IMP PMID:26634652 Valve Endothelial Cell-Derived TgfΞ²1 Signaling Promotes Nucl... | KEEP AS NON CORE | Summary: aortic valve morphogenesis. Reason: GO:0003180 aortic valve morphogenesis captures the developmental/homeostatic consequence of TGF-beta-1 signaling in the valve, not its molecular activity. The paper shows that valve endothelial cell-derived Tgfb1 maintains Sox9 in valve interstitial cells and that its loss leads to calcific aortic valve disease, i.e. the morphogenetic/homeostatic phenotype is a downstream outcome of TGFBR1/2 engagement and SMAD signaling rather than a function the ligand performs directly. Keep as non-core: this tissue-level valve role is one of many pleiotropic contexts entrained by the core receptor-binding function. The cached abstract frames the role as calcification/disease rather than morphogenesis per se, so the specific morphogenesis term rests on the uncited full text. |
| GO:0005114 type II transforming growth factor beta receptor binding | IDA PMID:11157754 Type III TGF-beta receptor-independent signalling of TGF-bet... | ACCEPT | Summary: Type II TGF-beta receptor binding. Reason: Core receptor-binding function. |
| GO:0005114 type II transforming growth factor beta receptor binding | IEA GO_REF:0000117 | ACCEPT | Summary: Type II TGF-beta receptor binding. Reason: Core receptor-binding function. |
| GO:0005114 type II transforming growth factor beta receptor binding | IMP PMID:8167376 Cloning and developmental expression of the chick type II an... | ACCEPT | Summary: Type II TGF-beta receptor binding. Reason: Core receptor-binding function. |
| GO:0005114 type II transforming growth factor beta receptor binding | IPI PMID:1333888 TGF beta signals through a heteromeric protein kinase recept... | ACCEPT | Summary: Type II TGF-beta receptor binding. Reason: Core receptor-binding function. |
| GO:0005125 cytokine activity | IBA GO_REF:0000033 | ACCEPT | Summary: Cytokine activity - TGF-beta-1 is a secreted cytokine. Reason: Core molecular function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Multifunctional protein that regulates the growth and differentiation of various cell types |
| GO:0005125 cytokine activity | IDA PMID:26572508 Rotavirus-induced miR-142-5p elicits proviral milieu by targ... | ACCEPT | Summary: Cytokine activity - TGF-beta-1 is a secreted cytokine. Reason: Core molecular function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Multifunctional protein that regulates the growth and differentiation of various cell types |
| GO:0005125 cytokine activity | IDA PMID:32644293 The deubiquitinase USP44 promotes Treg function during infla... | ACCEPT | Summary: Cytokine activity - TGF-beta-1 is a secreted cytokine. Reason: Core molecular function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Multifunctional protein that regulates the growth and differentiation of various cell types |
| GO:0005125 cytokine activity | TAS PMID:24263861 HCV NS3 protease enhances liver fibrosis via binding to and ... | ACCEPT | Summary: Cytokine activity - TGF-beta-1 is a secreted cytokine. Reason: Core molecular function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Multifunctional protein that regulates the growth and differentiation of various cell types |
| GO:0005160 transforming growth factor beta receptor binding | IEA GO_REF:0000120 | ACCEPT | Summary: Transforming growth factor beta receptor binding. Reason: Core; the mature cytokine binds TGF-beta receptors. |
| GO:0005515 protein binding | IPI PMID:10092230 Requirement of type III TGF-beta receptor for endocardial ce... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:10746731 Betaglycan binds inhibin and can mediate functional antagoni... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:10885742 Activin receptor-like kinase 2 can mediate atrioventricular ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:10930463 Specific sequence motif of 8-Cys repeats of TGF-beta binding... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:10930463 Specific sequence motif of 8-Cys repeats of TGF-beta binding... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:10930463 Specific sequence motif of 8-Cys repeats of TGF-beta binding... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:11157754 Type III TGF-beta receptor-independent signalling of TGF-bet... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:11157754 Type III TGF-beta receptor-independent signalling of TGF-bet... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:1326540 Endoglin is a component of the transforming growth factor-be... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:1326540 Endoglin is a component of the transforming growth factor-be... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:1326540 Endoglin is a component of the transforming growth factor-be... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:15247411 Vasorin, a transforming growth factor beta-binding protein e... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:15864306 A functional SNP in CILP, encoding cartilage intermediate la... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:17827158 Mechanisms for asporin function and regulation in articular ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:18672106 Latent TGF-beta binding proteins (LTBPs)-1 and -3 coordinate... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:18672106 Latent TGF-beta binding proteins (LTBPs)-1 and -3 coordinate... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:19651619 GARP (LRRC32) is essential for the surface expression of lat... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:2022183 A role of the latent TGF-beta 1-binding protein in the assem... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20505824 Agrin binds BMP2, BMP4 and TGFbeta1. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20856203 Critical role of endoglin in tumor cell plasticity of Ewing ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20856203 Critical role of endoglin in tumor cell plasticity of Ewing ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20856203 Critical role of endoglin in tumor cell plasticity of Ewing ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20856203 Critical role of endoglin in tumor cell plasticity of Ewing ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20860622 DIP2 disco-interacting protein 2 homolog A (Drosophila) is a... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20860622 DIP2 disco-interacting protein 2 homolog A (Drosophila) is a... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:20860622 DIP2 disco-interacting protein 2 homolog A (Drosophila) is a... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:21054789 WFIKKN1 and WFIKKN2 bind growth factors TGFΞ²1, BMP2 and BMP4... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:2119582 Transforming growth factor-beta bound to soluble derivatives... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:21441952 SCUBE3 is an endogenous TGF-Ξ² receptor ligand and regulates ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:21677751 Latent TGF-Ξ² structure and activation. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:25241761 Using an in situ proximity ligation assay to systematically ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:25416956 A proteome-scale map of the human interactome network. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:25548275 Induction and activation of latent transforming growth facto... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:26918958 Genotype-Specific Interaction of Latent TGFΞ² Binding Protein... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:27339457 Functional consequence of fibulin-4 missense mutations assoc... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:28514442 Architecture of the human interactome defines protein commun... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:29909984 A Milieu Molecule for TGF-Ξ² Required for Microglia Function ... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:30361387 Structural basis of latent TGF-Ξ²1 presentation and activatio... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:32296183 A reference map of the human binary protein interactome. | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:33961781 Dual proteome-scale networks reveal cell-specific remodeling... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:35443807 Tenascin-X Mediates Flow-Induced Suppression of EndMT and At... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:35443807 Tenascin-X Mediates Flow-Induced Suppression of EndMT and At... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:40205054 Multimodal cell maps as a foundation for structural and func... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:7852346 The soluble exoplasmic domain of the type II transforming gr... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:8370410 Identification and expression of two forms of the human tran... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:8370410 Identification and expression of two forms of the human tran... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005515 protein binding | IPI PMID:8617200 Association of the small latent transforming growth factor-b... | REMOVE | Summary: Generic protein binding (IPI). Reason: GO:0005515 is uninformative about molecular function; removal follows the protein-binding policy and does not dispute the interaction. TGF-beta-1 informative binding is captured by TGF-beta receptor binding and the latency/activation partners. |
| GO:0005576 extracellular region | EXP PMID:17827158 Mechanisms for asporin function and regulation in articular ... | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | EXP PMID:29483653 Human TGF-Ξ²1 deficiency causes severe inflammatory bowel dis... | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | IBA GO_REF:0000033 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | IC PMID:32644293 The deubiquitinase USP44 promotes Treg function during infla... | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | IDA PMID:19734317 Mesenchymal stem cells produce Wnt isoforms and TGF-beta1 th... | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | IEA GO_REF:0000120 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-168865 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-170835 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-170843 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-170846 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-170850 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-170861 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-170868 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-173483 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-173512 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-177107 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2128994 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2160931 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2160932 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2160935 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2169046 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2395320 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2395328 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2395364 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-2731078 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-3304394 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-3642203 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-3645780 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-3656382 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-3656523 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-481007 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-6789615 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839358 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839363 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839368 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839377 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839378 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839390 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-9839402 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2128982 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2161160 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2161165 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2167872 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2167890 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2169036 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2169043 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2176393 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2176396 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2176427 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2176431 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2179307 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005576 extracellular region | TAS Reactome:R-NUL-2179313 | ACCEPT | Summary: Extracellular region - TGF-beta-1 is secreted into the extracellular space/matrix. Reason: Core secreted location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt SUBCELLULAR LOCATION: [Transforming growth factor beta-1]: Secreted |
| GO:0005634 nucleus | IDA PMID:18040277 TGF-beta1 and TGF-beta2 expression after traumatic human spi... | MARK AS OVER ANNOTATED | Summary: nucleus. Reason: TGF-beta-1 is a secreted cytokine routed through the ER-Golgi secretory pathway, so a standalone nucleus term is an over-annotation of its functional site. The cited reference (full text unavailable in our cache) is an immunohistochemical study of injured human spinal cord reporting cell-type-level expression (TGF-beta-1 detected within neurons, astrocytes and invading macrophages); such cell-type IHC does not resolve a subcellular nuclear compartment, so it does not ground a nucleus annotation. Supporting Evidence: PMID:18040277 detected within neurons, astrocytes and invading macrophages |
| GO:0005737 cytoplasm | IDA PMID:18040277 TGF-beta1 and TGF-beta2 expression after traumatic human spi... | MARK AS OVER ANNOTATED | Summary: cytoplasm. Reason: For a secreted cytokine whose biosynthetic route is the ER-Golgi secretory pathway, a generic cytoplasm term is an over-annotation better captured by Golgi and extracellular terms. The cited reference (full text unavailable in our cache) is a cell-type-level immunohistochemical study of injured spinal cord (TGF-beta-1 detected within neurons, astrocytes and invading macrophages); such cell-type IHC does not resolve a free cytosolic pool at subcellular resolution. Supporting Evidence: PMID:18040277 detected within neurons, astrocytes and invading macrophages |
| GO:0005737 cytoplasm | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: cytoplasm. Reason: Electronic transfer from the mouse ortholog; a generic cytoplasm term is an over-annotation for a secreted cytokine whose route is the ER-Golgi secretory pathway, not the free cytosol. |
| GO:0005796 Golgi lumen | TAS Reactome:R-HSA-170844 | KEEP AS NON CORE | Summary: Golgi lumen. Reason: Biosynthetic transit compartment of the secreted protein, where the proprotein is cleaved by FURIN into the latency-associated peptide and the mature TGF-beta-1 chain; a real but non-core location en route to secretion. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt following cleavage of the proprotein in the Golgi apparatus |
| GO:0005796 Golgi lumen | TAS Reactome:R-HSA-177107 | KEEP AS NON CORE | Summary: Golgi lumen. Reason: Biosynthetic transit compartment of the secreted protein, where the proprotein is cleaved by FURIN into the latency-associated peptide and the mature TGF-beta-1 chain; a real but non-core location en route to secretion. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt following cleavage of the proprotein in the Golgi apparatus |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-168865 | KEEP AS NON CORE | Summary: plasma membrane. Reason: The latent TGF-beta-1 complex is presented at the cell surface by GARP (LRRC32), and the active cytokine engages its type I/II receptors at the plasma membrane; a real but non-core surface location upstream of the core receptor-binding function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt controls activation of TGF-beta-1 on the surface of |
| GO:0005886 plasma membrane | TAS Reactome:R-HSA-8870732 | KEEP AS NON CORE | Summary: plasma membrane. Reason: The latent TGF-beta-1 complex is presented at the cell surface by GARP (LRRC32), and the active cytokine engages its type I/II receptors at the plasma membrane; a real but non-core surface location upstream of the core receptor-binding function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt controls activation of TGF-beta-1 on the surface of |
| GO:0005902 microvillus | IDA PMID:19366691 Transforming growth factor beta1 signaling via interaction w... | KEEP AS NON CORE | Summary: microvillus. Reason: TGF-beta-1 localizes to microvilli where it engages cell-surface Hyal-2 (shown by immunoelectron microscopy); a real but non-core microvillar surface location of the secreted cytokine. Supporting Evidence: PMID:19366691 bound cell surface hyaluronidase Hyal-2 on microvilli |
| GO:0006611 protein export from nucleus | IDA PMID:17438144 Smad7 antagonizes transforming growth factor beta signaling ... | MARK AS OVER ANNOTATED | Summary: protein export from nucleus. Reason: GO:0006611 protein export from nucleus. This Smad7-focused study reports that in COS1/COS7 cells TGF-beta-1 treatment triggers relocation of the inhibitory Smad7 from the nucleus to the cytoplasm. TGF-beta-1 does not itself execute nuclear export; it is the extracellular ligand whose receptor binding and SMAD signaling indirectly cause Smad7 nucleocytoplasmic redistribution, and the paper notes this behaviour is cell-type dependent (it does not occur in Hep3B/HeLa cells). Over-annotation because the nuclear-export phenotype is a far-downstream, cell-type-restricted consequence of TGF-beta-1 signaling that the ligand does not itself perform, not a molecular activity of the cytokine or a canonical signaling step it carries out. Supporting Evidence: PMID:17438144 TGF-Ξ² treatment led to translocation of Smad7 to the cytoplasm in COS1 cells |
| GO:0006754 ATP biosynthetic process | IDA PMID:10513816 Differential mechanisms of inorganic pyrophosphate productio... | MARK AS OVER ANNOTATED | Summary: ATP biosynthetic process (IDA). Reason: TGF-beta-1 is a secreted signaling ligand; it modulates cellular metabolism indirectly but does not itself perform this metabolic/biosynthetic process. The term fails the participation test. |
| GO:0006796 phosphate-containing compound metabolic process | IDA PMID:10513816 Differential mechanisms of inorganic pyrophosphate productio... | MARK AS OVER ANNOTATED | Summary: phosphate-containing compound metabolic process (IDA). Reason: TGF-beta-1 is a secreted signaling ligand; it modulates cellular metabolism indirectly but does not itself perform this metabolic/biosynthetic process. The term fails the participation test. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IBA GO_REF:0000033 | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:11157754 Type III TGF-beta receptor-independent signalling of TGF-bet... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:12574355 Human activation-induced cytidine deaminase is induced by IL... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:15334054 Hepatitis C viral proteins interact with Smad3 and different... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:18453574 Activation of a TGF-beta-specific multistep gene expression ... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:18593713 Smad7 stabilizes beta-catenin binding to E-cadherin complex ... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:18625725 Transforming growth factor beta engages TACE and ErbB3 to ac... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:19736306 Endoglin phosphorylation by ALK2 contributes to the regulati... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:26572508 Rotavirus-induced miR-142-5p elicits proviral milieu by targ... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:27693460 Vascular mimicry formation is promoted by paracrine TGF-Ξ² an... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:28373289 miR-202 Diminishes TGFΞ² Receptors and Attenuates TGFΞ²1-Induc... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:28467929 PPARΞ³ Links BMP2 and TGFΞ²1 Pathways in Vascular Smooth Muscl... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:31023188 LRP1 Deficiency in Vascular SMC Leads to Pulmonary Arterial ... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:32644293 The deubiquitinase USP44 promotes Treg function during infla... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IDA PMID:9389648 Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-indu... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IEA GO_REF:0000107 | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IGI PMID:22714950 MicroRNA-181a regulates local immune balance by inhibiting p... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IMP PMID:25196641 Inhibition of TGF-Ξ²/SMAD3/NF-ΞΊB signaling by microRNA-491 is... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IMP PMID:26908446 MicroRNA-323-3p inhibits cell invasion and metastasis in pan... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | IMP PMID:31368162 HIF1A/miR-20a-5p/TGFΞ²1 axis modulates adipose-derived stem c... | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007179 transforming growth factor beta receptor signaling pathway | ISS GO_REF:0000024 | ACCEPT | Summary: Transforming growth factor beta receptor signaling pathway. Reason: Core signaling pathway initiated by TGF-beta-1. |
| GO:0007249 canonical NF-kappaB signal transduction | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: canonical NF-kappaB signal transduction. Reason: canonical NF-kappaB signal transduction is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0007406 negative regulation of neuroblast proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of neuroblast proliferation. Reason: negative regulation of neuroblast proliferation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0007435 salivary gland morphogenesis | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: salivary gland morphogenesis. Reason: salivary gland morphogenesis is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0007435 salivary gland morphogenesis | IEP PMID:18080134 Developing human minor salivary glands: morphological parall... | KEEP AS NON CORE | Summary: salivary gland morphogenesis. Reason: GO:0007435 salivary gland morphogenesis is an IEP (expression-pattern) annotation: TGF-beta-1 protein is spatially and temporally expressed during human minor salivary gland development, first appearing at the canalisation stage in surrounding mesenchyme and later in acinar cells. The inferred developmental role is a downstream morphogenetic consequence of secreted-ligand signaling to receptors, so it is non-core. The expression correlation supports a developmental role but not a direct molecular activity. Supporting Evidence: PMID:18080134 TGF-beta 1 first appeared during canalisation stage in the surrounding mesenchyme |
| GO:0007507 heart development | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: heart development. Reason: heart development is a phylogenetic (PAINT) inference propagated across the TGF-beta ligand family (IBA, GO_REF:0000033). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0007507 heart development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: heart development. Reason: heart development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0007507 heart development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: heart development. Reason: heart development is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0007565 female pregnancy | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: female pregnancy. Reason: female pregnancy is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 influences this process indirectly through receptor binding and SMAD-dependent signaling in target cells; a genuine but downstream, non-core consequence of the pleiotropic secreted cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0008083 growth factor activity | IEA GO_REF:0000002 | ACCEPT | Summary: Growth factor activity. Reason: Core molecular function; TGF-beta-1 regulates growth and differentiation. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Multifunctional protein that regulates the growth and differentiation of various cell types |
| GO:0008083 growth factor activity | IMP PMID:31368162 HIF1A/miR-20a-5p/TGFΞ²1 axis modulates adipose-derived stem c... | ACCEPT | Summary: Growth factor activity. Reason: Core molecular function; TGF-beta-1 regulates growth and differentiation. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Multifunctional protein that regulates the growth and differentiation of various cell types |
| GO:0008284 positive regulation of cell population proliferation | IDA PMID:10513816 Differential mechanisms of inorganic pyrophosphate productio... | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation. Reason: Annotates TGF-beta-1 to positive regulation of cell proliferation (IDA). The cited paper concerns TGF-beta-inducible plasma-cell membrane glycoprotein-1 (PC-1/ENPP1) and inorganic pyrophosphate production in chondrocytes; its abstract does not itself address TGF-beta-1 promoting cell proliferation. TGF-beta-1 can be mitogenic in certain mesenchymal contexts, but that is a context-specific downstream signaling output and thus non-core. The abstract provides no verbatim support for the proliferation term, so the claim rests on the uncached full text; no quote is asserted. |
| GO:0008284 positive regulation of cell population proliferation | IDA PMID:14633705 SB-431542 and Gleevec inhibit transforming growth factor-bet... | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation. Reason: GO:0008284 positive regulation of cell population proliferation reflects the context-dependent growth-stimulating action of TGF-beta1 on mesenchymal and tumour cells, here on MG63 osteosarcoma cells where ALK5/SMAD signaling induces PDGF-AA and upregulates c-Myc to drive proliferation. This proliferative output is opposite in sign to TGF-beta1's usual cytostatic effect and is a cell-type-specific downstream response to receptor binding, peripheral to the core cytokine activity, so it is non-core. Supporting Evidence: PMID:14633705 Transforming growth factor-beta (TGF-beta) has growth-stimulating effects on mesenchymal cells and several tumor cell lines |
| GO:0008284 positive regulation of cell population proliferation | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation. Reason: positive regulation of cell population proliferation is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0008284 positive regulation of cell population proliferation | IMP PMID:26169693 miR-208-3p promotes hepatocellular carcinoma cell proliferat... | KEEP AS NON CORE | Summary: positive regulation of cell population proliferation. Reason: Positive regulation of cell population proliferation is supported by loss-of-function data in hepatocellular carcinoma: depleting TGF-beta1 reduced HCC colony-formation ability, an effect reversed by the downstream effector miR-208-3p. TGF-beta1 promotes proliferation here indirectly, through the TGFB1/miR-208-3p/ARID2 axis, a cancer-context downstream consequence of its signaling rather than a core molecular function of the cytokine, so it is retained as non-core. Supporting Evidence: PMID:26169693 depeted TGFΞ²1 inhibited HCC cell invasion and colony formation ability |
| GO:0008285 negative regulation of cell population proliferation | IDA PMID:14555988 Differential regulation of TGF-beta signaling through Smad2,... | KEEP AS NON CORE | Summary: negative regulation of cell population proliferation. Reason: Annotates TGF-beta-1 to negative regulation of cell proliferation (IDA). The paper establishes that Smad transcription factors (predominantly Smad3) mediate the growth-inhibitory effect of TGF-beta on keratinocytes, including cell-cycle arrest. The antiproliferative response is a downstream transcriptional output of TGF-beta-1 receptor/SMAD signaling, so it is non-core relative to the ligand's receptor-binding function. Supporting Evidence: PMID:14555988 growth inhibitory effect of transforming growth factor-beta |
| GO:0008285 negative regulation of cell population proliferation | IDA PMID:15334054 Hepatitis C viral proteins interact with Smad3 and different... | KEEP AS NON CORE | Summary: negative regulation of cell population proliferation. Reason: Annotates TGF-beta-1 to negative regulation of cell proliferation. This paper shows TGF-beta/Smad3 signaling imposes a G1-phase arrest (via p21 induction) that HCV core protein can repress. The cytostatic effect is a canonical transcriptional output of TGF-beta-1 binding TGFBR1/2 and activating Smad3, i.e. a downstream consequence of the receptor/SMAD cascade rather than the ligand's own molecular activity, so it is non-core. Supporting Evidence: PMID:15334054 represses TGF-beta-induced G1 phase arrest |
| GO:0008285 negative regulation of cell population proliferation | IMP PMID:11158066 Human leiomyoma smooth muscle cells show increased expressio... | KEEP AS NON CORE | Summary: negative regulation of cell population proliferation. Reason: Annotates TGF-beta-1 to negative regulation of cell proliferation (IMP). In myometrial smooth muscle cells TGF-beta-1 inhibited DNA synthesis by 31-54%, an antiproliferative effect reversed by a neutralizing antibody. This cytostatic response is a downstream outcome of TGF-beta-1 receptor engagement and SMAD signaling in a specific cell type, so it is non-core to the ligand's core receptor-binding function. Supporting Evidence: PMID:11158066 TGF beta 1 and TGF beta 3 inhibited DNA synthesis in myometrium smooth muscle cells |
| GO:0009410 response to xenobiotic stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to xenobiotic stimulus. Reason: response to xenobiotic stimulus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of xenobiotic stimulus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0009611 response to wounding | IEP PMID:18040277 TGF-beta1 and TGF-beta2 expression after traumatic human spi... | KEEP AS NON CORE | Summary: response to wounding. Reason: GO:0009611 response to wounding. PMID:18040277 shows TGF-beta1 immunoreactivity is dramatically upregulated within 2 days of traumatic human spinal cord injury (IEP), i.e. its expression responds to wounding, with the authors attributing it to the acute inflammatory response and glial-scar formation. This is an expression/context-based downstream role of the injured tissue, not a core molecular activity of the ligand. Supporting Evidence: PMID:18040277 TGF-beta1 immunoreactivity was dramatically upregulated by 2 days after injury |
| GO:0009749 response to glucose | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to glucose. Reason: response to glucose is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of glucose; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0009986 cell surface | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cell surface. Reason: The GARP (LRRC32), LTBP and NRROS machinery tethers the latent TGF-beta-1 complex at the cell surface (for example on platelets and FOXP3+ regulatory T cells); a real but non-core presentation location upstream of the secreted cytokine's core receptor-binding/SMAD-signaling function. Supporting Evidence: PMID:19651619 activated Tregs co-express latent TGF-beta and GARP on their membranes |
| GO:0009986 cell surface | IMP PMID:19366691 Transforming growth factor beta1 signaling via interaction w... | KEEP AS NON CORE | Summary: cell surface. Reason: On receptor-deficient HCT116 cells, cell-surface TGF-beta-1 engages the microvillar hyaluronidase Hyal-2 and recruits WOX1, a surface interaction distinct from the GARP-tethered latent pool; a real but non-core surface location of the secreted cytokine. Supporting Evidence: PMID:19366691 bound cell surface hyaluronidase Hyal-2 on microvilli |
| GO:0010332 response to gamma radiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to gamma radiation. Reason: response to gamma radiation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of gamma radiation; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0010575 positive regulation of vascular endothelial growth factor production | TAS PMID:19506300 Expression of vascular endothelial growth factor is coordina... | KEEP AS NON CORE | Summary: positive regulation of vascular endothelial growth factor production. Reason: GO:0010575 positive regulation of vascular endothelial growth factor production. In aortic endothelial cells TGF-beta-1 upregulates VEGF expression through the ALK5/TGFBR2/SMAD2 arm (antagonized by BMP-9/ALK1/SMAD1), establishing TGF-beta-1 as a positive regulator of VEGF in the endothelium. This is a downstream transcriptional output of the core receptor-binding + SMAD2 signaling function: TGF-beta-1 is the initiating ligand and the VEGF promoter response is executed by SMAD transcription factors, not by the cytokine directly. Non-core because VEGF induction is one context-specific (endothelial/angiogenic) downstream effect of TGF-beta-1 signaling rather than its core molecular activity. Supporting Evidence: PMID:19506300 TGFΞ²1 stimulated VEGF expression by activating ALK5, TGFΞ² type II receptor, and SMAD2 |
| GO:0010628 positive regulation of gene expression | IDA PMID:18625725 Transforming growth factor beta engages TACE and ErbB3 to ac... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. In HER2-overexpressing breast cells (PMID:18625725) activated TGF-beta/Alk5 signaling induces a transcriptional gene signature, consistent with TGF-beta1's general transcriptional output through SMADs. This is a very broad downstream term, not a core molecular activity. The abstract attributes the induced gene signature to the activated receptor (Alk5 T204D) rather than stating a specific TGF-beta1-driven gene-expression event, so the specific claim rests on the curator's full-text reading (not cached). |
| GO:0010628 positive regulation of gene expression | IDA PMID:18832382 HMGA2 and Smads co-regulate SNAIL1 expression during inducti... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression here reflects the TGF-beta1/SMAD pathway cooperating with HMGA2 to upregulate SNAIL1 expression during EMT. This is a transcriptional output of the pathway, downstream of receptor binding and SMAD nuclear translocation, and is a generic consequence of signaling rather than the core cytokine activity, so it is non-core. Supporting Evidence: PMID:18832382 HMGA2 cooperates with the TGF-beta/Smad pathway in regulating SNAIL1 gene expression |
| GO:0010628 positive regulation of gene expression | IDA PMID:18941241 IL-4-induced selective clearance of oligomeric beta-amyloid ... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. The cached abstract of PMID:18941241 is about IL-4-induced CD36/neprilysin/IDE expression and amyloid-beta clearance in rat primary microglia and does not mention TGF-beta1; the general positive-regulation-of-gene-expression annotation to TGFB1 therefore rests on full-text data (not cached). This is a very broad downstream SMAD-mediated term, not a core molecular activity. The annotation is retained rather than removed given the full text is unavailable. |
| GO:0010628 positive regulation of gene expression | IDA PMID:19913496 Suppression of type I collagen production by microRNA-29b in... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression reflects TGF-beta-1 altering expression of target genes/miRNAs in hepatic stellate cells, part of the pro-fibrotic program (e.g. type I collagen induction). The cached abstract states that miR-29b/-143/-218 expression is altered in response to TGF-beta-1 but does not specify the upregulated target supporting the positive direction, so that rests on the uncited full text. As a transcriptional output of SMAD signaling it is a downstream, non-core consequence of receptor binding. |
| GO:0010628 positive regulation of gene expression | IDA PMID:25322725 MicroRNA-34a regulates cardiac fibrosis after myocardial inf... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. PMID:25322725 shows TGF-beta1 increases miR-34a expression in cardiac fibroblasts, a concrete instance of positively regulating gene (microRNA) expression downstream of Smad signaling in the post-infarction fibrotic context. Positive regulation of gene expression is a broad downstream term, not a core molecular activity of the ligand. Supporting Evidence: PMID:25322725 TGF-Ξ²1 increased miR-34a expression in cardiac fibroblasts. |
| GO:0010628 positive regulation of gene expression | IDA PMID:26634652 Valve Endothelial Cell-Derived TgfΞ²1 Signaling Promotes Nucl... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression here reflects TGF-beta-1 promoting expression of SOX9 in valve interstitial cells; endothelial Tgfb1 loss reduces Sox9 expression. This is a transcriptional output of canonical TGFBR/SMAD signaling, a downstream consequence of the core receptor-binding function, so it is non-core. It is kept because the directional (positive) effect on a target gene is supported, but it is one tissue-specific instance of the ligand's broad transcriptional influence. Supporting Evidence: PMID:26634652 loss of TgfΞ²1 in the endothelium leads to reduced Sox9 expression and calcific aortic valve disease |
| GO:0010628 positive regulation of gene expression | IDA PMID:26687115 The microRNA-29 family in cartilage homeostasis and osteoart... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. In this chondrocyte/osteoarthritis study the specific, directly measured TGF-beta-1 effect is a DECREASE in miR-29a/b/c expression (i.e. negative regulation of those miRNA genes), not a positive effect, so the paper does not directly substantiate a positive-direction gene-expression term for TGF-beta-1 (any positive consequence would be indirect de-repression of miR-29 targets). Whatever the direction, regulation of target-gene expression is a downstream transcriptional output of the core receptor-binding + SMAD signaling pathway, executed by SMAD transcription factors, and is tissue/context-specific (cartilage). Non-core; no verbatim text supports the positive-direction claim, so no supporting quote is provided. |
| GO:0010628 positive regulation of gene expression | IDA PMID:27162619 Regulation and function of miR-214 in pulmonary arterial hyp... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. In pulmonary artery smooth muscle cells TGF-beta-1 induces transcription of the pri-miR-199/214 cluster and raises all four mature miRNAs, an effect abolished by the ALK5 inhibitor SB525334, confirming it is mediated by canonical TGF-beta receptor/SMAD signaling. This positive effect on specific target genes is a downstream transcriptional output of the core receptor-binding + SMAD function (SMAD transcription factors act at the miR-199/214 promoter), with TGF-beta-1 acting as the upstream ligand. Non-core because it is one context-specific (PASMC/pulmonary hypertension) consequence of TGF-beta-1 signaling, not a core molecular activity of the cytokine. Supporting Evidence: PMID:27162619 TGF-Ξ²1 increased the expression of pri-miR-199/214 in PASMCs |
| GO:0010628 positive regulation of gene expression | IDA PMID:28467929 PPARΞ³ Links BMP2 and TGFΞ²1 Pathways in Vascular Smooth Muscl... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: Annotates TGF-beta-1 to positive regulation of gene expression. In vascular smooth muscle cells, TGF-beta-1 induces fibrosis-related genes and the miR-130a/301b cluster. Gene induction is a transcriptional output of the TGF-beta-1-Smad3/4 (and Stat3) cascade activated after receptor binding, so this upregulatory activity is a downstream, non-core effect of the ligand's core receptor-binding/signal-initiating role. Supporting Evidence: PMID:28467929 TGFΞ²1 induces fibrosis-related genes and miR-130a/301b |
| GO:0010628 positive regulation of gene expression | IDA PMID:29167509 Cartilage intermediate layer protein 1 (CILP1): A novel medi... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. In human (myo)fibroblasts TGF-Ξ²1 upregulated pro-fibrotic/ECM genes, increasing Ξ±-SMA and producing a clear induction of COL1A1 and CTGF. This upregulation is the downstream SMAD-dependent transcriptional output of TGFB1 signaling in the responding fibroblast, not a molecular activity the secreted ligand performs itself, so it is a non-core consequence of TGFB1's core receptor-binding/SMAD-initiating role. Supporting Evidence: PMID:29167509 clear TGFΞ²1-induced increase of COL1A1 and CTGF expression |
| GO:0010628 positive regulation of gene expression | IDA PMID:31694982 Long noncoding RNA DNM3OS promotes prostate stromal cells tr... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: GO:0010628 positive regulation of gene expression. In prostate stromal cells undergoing myofibroblast transformation, TGF-beta-1 stimulation increases COL3A1 (and the lncRNA DNM3OS) expression, an effect reproduced/blocked by the TGFBR1 inhibitor SB431542, showing it works through canonical TGF-beta receptor/SMAD2 signaling. Upregulation of these ECM/fibrosis genes is a downstream transcriptional output executed by SMAD transcription factors, with TGF-beta-1 serving as the upstream secreted ligand. Non-core because it is a context-specific (prostate stroma/BPH fibrosis) consequence of the core receptor-binding + SMAD signaling function rather than that function itself. Supporting Evidence: PMID:31694982 TGFΞ²1 stimulation significantly increased the protein level of COL3A1 |
| GO:0010628 positive regulation of gene expression | IGI PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: Positive regulation of gene expression here refers to TGF-beta-1 raising collagen gene/mRNA levels in aortic fibroblasts. In this AAA study TGF-beta1 was applied as a profibrotic stimulus and increased collagen synthesis in treated cells; the derepression of collagen genes works partly via repression of miR-29b. This is a downstream transcriptional consequence of TGFBR1/2 binding and SMAD signaling in a specific vascular cell context, not a molecular activity TGF-beta-1 itself carries out, so it is correctly non-core. Supporting Evidence: PMID:22269326 Collagen synthesis was increased in TGF-Ξ²1βtreated cells compared with that in an untreated control group. |
| GO:0010628 positive regulation of gene expression | IMP PMID:26169693 miR-208-3p promotes hepatocellular carcinoma cell proliferat... | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: Positive regulation of gene expression here is TGF-beta-1 inducing the microRNA miR-208-3p: silencing TGFB1 lowered miR-208-3p, and TGF-beta1 is placed upstream as its activator in the TGFB1/miR-208-3p/ARID2 pathway. Upregulating a downstream miRNA is a transcriptional output of TGF-beta signaling several steps from receptor binding, not a core molecular activity, so non-core is correct. Supporting Evidence: PMID:26169693 repress TGFΞ²1 expression, repress miR-208-3p expression, and upregulate the protein level of ARID2 and IFITM1 |
| GO:0010628 positive regulation of gene expression | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: positive regulation of gene expression. Reason: positive regulation of gene expression is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). this transcriptional/expression effect is the downstream output of TGF-beta-1 receptor binding and SMAD activation in responding cells, not an activity the ligand itself executes; retained as a genuine but non-core regulatory consequence. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0010629 negative regulation of gene expression | IDA PMID:19913496 Suppression of type I collagen production by microRNA-29b in... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: GO:0010629 negative regulation of gene expression reflects TGF-beta-1 downregulating a target (plausibly anti-fibrotic miR-29b, whose suppression de-represses type I collagen) in hepatic stellate cells. The abstract notes TGF-beta-1 alters miR-29b expression but does not state the repressive direction for a named target, so this negative-direction annotation rests on the uncited full text. It is a downstream transcriptional consequence of SMAD signaling and therefore non-core. |
| GO:0010629 negative regulation of gene expression | IDA PMID:20067797 High glucose down-regulates miR-29a to increase collagen IV ... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: GO:0010629 negative regulation of gene expression reflects high-glucose/TGF-beta1 signaling downregulating the microRNA miR-29a in proximal tubule cells, which de-represses collagen IV (col4a1/col4a2) and drives profibrotic matrix deposition in diabetic nephropathy. This is a specific expression output downstream of TGF-beta1/SMAD signaling, a disease-context regulatory effect peripheral to the core receptor-binding function, hence non-core. Supporting Evidence: PMID:20067797 high glucose/TGF-beta1 induced significant down-regulation of miR-29a |
| GO:0010629 negative regulation of gene expression | IDA PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: Negative regulation of gene expression is grounded in TGF-beta-1 lowering the level of a specific gene product (miR-29b) in human aortic adventitial fibroblasts. TGF-beta1 treatment significantly decreased miR-29b, which in turn derepresses its collagen/ECM targets. This repression is an indirect, cell-type-specific output of canonical TGF-beta signaling rather than a core molecular function of the secreted ligand, so non-core is appropriate. Supporting Evidence: PMID:22269326 Treatment with TGF-Ξ²1 significantly decreased miR-29b expression in hAFBs but not in hASMCs |
| GO:0010629 negative regulation of gene expression | IDA PMID:25163461 Inhibitory effect of hsa-miR-590-5p on cardiosphere-derived ... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: GO:0010629 negative regulation of gene expression reflects TGF-beta1 downregulating the microRNA miR-590 during cardiac differentiation of cardiosphere-derived cells, which in turn de-represses TGFBR2. This is a specific transcriptional/expression output downstream of TGF-beta1/SMAD signaling (part of a feed-forward loop reinforcing its own receptor), peripheral to the core cytokine-receptor binding activity, so it is non-core. Supporting Evidence: PMID:25163461 TGFB1 exerts its differentiation induction via downregulation of miR-590 |
| GO:0010629 negative regulation of gene expression | IDA PMID:26634652 Valve Endothelial Cell-Derived TgfΞ²1 Signaling Promotes Nucl... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: GO:0010629 negative regulation of gene expression reflects TGF-beta-1 repressing a target gene in the valve interstitial cell context studied here; the abstract documents the positive Sox9 arm and the calcification phenotype but does not name a gene that Tgfb1 downregulates. As a transcriptional output of SMAD signaling it is a downstream, context-specific consequence of the core receptor-binding function and is non-core. The specific repressed target substantiating this negative-direction annotation is in the uncited full text, not the cached abstract. |
| GO:0010629 negative regulation of gene expression | IDA PMID:28467929 PPARΞ³ Links BMP2 and TGFΞ²1 Pathways in Vascular Smooth Muscl... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: Annotates TGF-beta-1 to negative regulation of gene expression. The paper shows TGF-beta-1 (via induced miR-130a/301b) suppresses PPARgamma expression in vascular smooth muscle cells. This repressive effect is mediated by the TGF-beta-1-triggered signaling cascade (SMAD/microRNA relay) acting downstream of receptor binding, making it a non-core consequence rather than the ligand's intrinsic activity. Supporting Evidence: PMID:28467929 miR-130a/301b, suppressing PPARΞ³ |
| GO:0010629 negative regulation of gene expression | IDA PMID:29167509 Cartilage intermediate layer protein 1 (CILP1): A novel medi... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: GO:0010629 negative regulation of gene expression. The same study shows that in rat cardiac ventricular fibroblasts TGF-Ξ²1, while inducing Ξ±-SMA, repressed CILP1 expression (an effect confirmed as TGFΞ²-dependent via a TΞ²RI inhibitor). This gene downregulation is a cell-type-specific downstream transcriptional consequence of TGFB1/SMAD signaling in the target cell rather than a direct molecular activity of the ligand, hence peripheral to the core function. Supporting Evidence: PMID:29167509 TGFΞ²1 increased Ξ±SMA expression, but inhibited CILP1 expression in CFB |
| GO:0010629 negative regulation of gene expression | IDA PMID:29529050 Transmembrane protease, serine 4 (TMPRSS4) is upregulated in... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: GO:0010629 negative regulation of gene expression. The paper shows TGF-Ξ²1 produces a strong decrease in E-cadherin in A549 epithelial cells (used as the EMT positive control), i.e. it represses E-cadherin expression. This downregulation is an indirect downstream output of SMAD-dependent transcriptional reprogramming during EMT rather than a direct molecular activity of the secreted TGFB1 ligand, so it is peripheral to TGFB1's core receptor-binding/signal-initiating function. Supporting Evidence: PMID:29529050 TMPRSS4 partially inhibited the strong decrease of E-cadherin induced by TGF-Ξ²1 |
| GO:0010629 negative regulation of gene expression | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: negative regulation of gene expression is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this transcriptional/expression effect is the downstream output of TGF-beta-1 receptor binding and SMAD activation in responding cells, not an activity the ligand itself executes; retained as a genuine but non-core regulatory consequence. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0010629 negative regulation of gene expression | IGI PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: This row again captures TGF-beta-1 repressing the microRNA miR-29b in aortic fibroblasts, shown via combined TGF-beta1 stimulation and miR-29b modulation (genetic interaction). Repressing a downstream miRNA is a context-specific signaling consequence several steps removed from receptor binding and SMAD activation, not a core activity of the cytokine, and is therefore kept as non-core. Supporting Evidence: PMID:22269326 Treatment with TGF-Ξ²1 significantly decreased miR-29b expression in hAFBs but not in hASMCs |
| GO:0010629 negative regulation of gene expression | IGI PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: A duplicate genetic-interaction assertion that TGF-beta-1 negatively regulates expression of miR-29b in the aortic-fibroblast AAA model; it reinforces row 229 rather than adding a distinct function. The effect is a downstream, tissue-specific modulation of a target gene product via SMAD signaling, not a core molecular function, so it stays non-core. Supporting Evidence: PMID:22269326 Treatment with TGF-Ξ²1 significantly decreased miR-29b expression in hAFBs but not in hASMCs |
| GO:0010629 negative regulation of gene expression | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: negative regulation of gene expression. Reason: negative regulation of gene expression is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). this transcriptional/expression effect is the downstream output of TGF-beta-1 receptor binding and SMAD activation in responding cells, not an activity the ligand itself executes; retained as a genuine but non-core regulatory consequence. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0010716 negative regulation of extracellular matrix disassembly | TAS PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: negative regulation of extracellular matrix disassembly. Reason: Negative regulation of extracellular matrix disassembly reflects the net antiproteolytic/profibrotic outcome of the TGF-beta1-miR-29b axis: by repressing miR-29b (and thereby altering its MMP2/MMP9 and collagen targets) TGF-beta1 favors matrix accumulation over degradation in the aortic wall. This is an inferred pathway-level (TAS) consequence of TGF-beta signaling in vascular remodeling, not a direct molecular activity of the ligand; the paper documents the miR-29b/MMP/collagen biology but does not contain a sentence tying TGF-beta-1 itself to inhibition of ECM disassembly, so no quote is asserted. Non-core. |
| GO:0010718 positive regulation of epithelial to mesenchymal transition | IDA PMID:17999987 Loss of type III transforming growth factor beta receptor ex... | KEEP AS NON CORE | Summary: positive regulation of epithelial to mesenchymal transition. Reason: GO:0010718 positive regulation of epithelial to mesenchymal transition reflects the well-established role of the TGF-beta signaling pathway as a key driver of EMT, the setting of this pancreatic-cancer study (which centres on loss of the type III receptor TbetaRIII modulating EMT-associated motility). TGF-beta1-induced EMT is a downstream morphogenetic program executed after receptor binding and SMAD/SNAIL activation, context-specific to development and tumour progression, so it is peripheral to the core receptor-binding function and kept as non-core (the abstract supports TGF-beta as an EMT regulator; the positive direction is established pathway biology detailed in the full text). Supporting Evidence: PMID:17999987 The transforming growth factor beta (TGF-beta) signaling pathway is a key regulator of EMT |
| GO:0010718 positive regulation of epithelial to mesenchymal transition | IDA PMID:18505915 Transforming growth factor-beta1, transforming growth factor... | KEEP AS NON CORE | Summary: positive regulation of epithelial to mesenchymal transition. Reason: GO:0010718 positive regulation of epithelial to mesenchymal transition is supported by TGF-beta-1 (with -beta2/-beta3) inducing a Smad3-dependent EMT in ovarian cancer cells (loss of cell-cell junctions, E-cadherin down, N-cadherin up). EMT induction is a canonical downstream program of TGFBR/SMAD3 signaling, a consequence of the core receptor-binding function, so it is non-core rather than the molecular activity itself. Supporting Evidence: PMID:18505915 enhance ovarian cancer metastatic potential by inducing a Smad3-dependent epithelial-to-mesenchymal transition |
| GO:0010718 positive regulation of epithelial to mesenchymal transition | IDA PMID:26572508 Rotavirus-induced miR-142-5p elicits proviral milieu by targ... | KEEP AS NON CORE | Summary: positive regulation of epithelial to mesenchymal transition. Reason: GO:0010718 positive regulation of epithelial to mesenchymal transition is supported by TGFbeta-induced EMT (and apoptosis) via non-canonical signaling in HT29 colon cells, which rotavirus-induced miR-142-5p blocks. EMT induction is a downstream consequence of TGFBR/SMAD engagement, so it is non-core relative to the ligand's core receptor-binding activity. The abstract attributes EMT to TGFbeta generically; TGF-beta-1-specific attribution rests on the uncited full text. Supporting Evidence: PMID:26572508 TGFΞ²-induced apoptosis and epithelial to mesenchymal transition |
| GO:0010718 positive regulation of epithelial to mesenchymal transition | IMP PMID:21490602 Multiple targets of miR-302 and miR-372 promote reprogrammin... | KEEP AS NON CORE | Summary: positive regulation of epithelial to mesenchymal transition. Reason: GO:0010718 positive regulation of epithelial to mesenchymal transition. The paper uses TGF-beta-1 (2 ng/ml) as the canonical inducer of EMT in HaCaT keratinocytes, driving SMAD2/3 phosphorylation, SLUG induction, loss of E-cadherin/ZO-1, and a mesenchymal morphology that miR-302b/372 (which repress TGFBR2) block. As the upstream ligand that initiates EMT, TGF-beta-1 positively regulates the transition, which is exactly what this term asserts (the transition itself is then executed downstream by SLUG/ZEB transcription factors). Kept non-core because promoting EMT is a context-specific downstream consequence of the core receptor-binding + SMAD function rather than a core molecular activity of the cytokine. Supporting Evidence: PMID:21490602 TGF-Ξ² can induce an EMT in epithelial cells |
| GO:0010718 positive regulation of epithelial to mesenchymal transition | NAS PMID:21319131 The role of bone morphogenetic protein-5 (BMP-5) in human ne... | KEEP AS NON CORE | Summary: positive regulation of epithelial to mesenchymal transition. Reason: GO:0010718 positive regulation of epithelial to mesenchymal transition. PMID:21319131 uses TGF-beta-induced EMT in HK-2 proximal tubular cells as an assay (attenuated by BMP-5) in the context of nephrosclerosis. TGF-beta1-driven EMT is a well-documented downstream morphogenetic/fibrotic program of Smad signaling, context-specific and non-core relative to receptor binding. The supporting evidence code here is NAS. Supporting Evidence: PMID:21319131 TGF-Γ-induced epithelial-to-mesenchymal transition (EMT) |
| GO:0010742 macrophage derived foam cell differentiation | IC PMID:15219857 Up-regulation of acyl-coenzyme A:cholesterol acyltransferase... | KEEP AS NON CORE | Summary: macrophage derived foam cell differentiation. Reason: GO:0010742 macrophage derived foam cell differentiation. PMID:15219857 shows TGF-beta1 upregulates ACAT-1 (cholesterol acyltransferase) during monocyte-to-macrophage differentiation; the curator inferred (IC) a contribution to foam-cell formation from this cholesterol-esterification effect, relevant to atherosclerotic lesions. This is an indirect, disease-context consequence of TGF-beta1 signaling. The cached abstract does not mention foam cells explicitly (the row is an IC inference), so that specific link rests on the curator's reasoning and full-text reading. |
| GO:0010763 positive regulation of fibroblast migration | IDA PMID:18555217 Differential involvement of TGF-beta1 in mediating the motog... | KEEP AS NON CORE | Summary: positive regulation of fibroblast migration. Reason: GO:0010763 positive regulation of fibroblast migration captures a motogenic output of TGF-beta1 in a transmembrane (Boyden) migration assay, where TGF-beta1 reproduced the dose-dependent stimulation of fibroblast migration seen with thrombospondin-1. This is a downstream cellular response elicited after TGF-beta1 binds TGFBR1/2 and activates SMAD signaling, not the receptor-binding event itself, and it is cell-type- and context-specific (fibroblast migration here was shown to be TGF-beta1-independent in the TSP-1 pathway), so it is peripheral to the core receptor-ligand function and correctly non-core. Supporting Evidence: PMID:18555217 TGF-beta1 (0.1-200 ng/ml tested) mimicked the effects of TSP-1 on cell migration |
| GO:0010936 negative regulation of macrophage cytokine production | IDA PMID:20875417 TGF-Ξ²2 suppresses macrophage cytokine production and mucosal... | KEEP AS NON CORE | Summary: negative regulation of macrophage cytokine production. Reason: GO:0010936 negative regulation of macrophage cytokine production. In the developing intestine TGF-beta suppresses LPS-induced macrophage pro-inflammatory cytokine (TNF-alpha/IL-8) production; the study attributes most of this activity to the TGF-beta2 isoform, with recombinant TGF-beta-1 producing a smaller but real suppressive effect. This anti-inflammatory suppression is a downstream immunomodulatory consequence of TGF-beta-1 receptor binding and SMAD2 signaling in a specific tissue/developmental context (fetal intestinal macrophage differentiation), not a core molecular activity of the cytokine, and TGF-beta-1 is not the dominant isoform here. Non-core; supporting text confirms TGF-beta (particularly the beta2 isoform) suppresses macrophage cytokine production. Supporting Evidence: PMID:20875417 Macrophage cytokine production was suppressed in the developing intestine by TGF-Ξ², particularly the TGF-Ξ²(2) isoform |
| GO:0010936 negative regulation of macrophage cytokine production | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: negative regulation of macrophage cytokine production. Reason: negative regulation of macrophage cytokine production is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0014003 oligodendrocyte development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: oligodendrocyte development. Reason: oligodendrocyte development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0014008 positive regulation of microglia differentiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of microglia differentiation. Reason: positive regulation of microglia differentiation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0014008 positive regulation of microglia differentiation | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: positive regulation of microglia differentiation. Reason: positive regulation of microglia differentiation is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0016202 regulation of striated muscle tissue development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: regulation of striated muscle tissue development. Reason: regulation of striated muscle tissue development is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0019899 enzyme binding | IPI PMID:19366691 Transforming growth factor beta1 signaling via interaction w... | KEEP AS NON CORE | Summary: enzyme binding. Reason: The IPI partner O35632 is the enzyme hyaluronidase Hyal-2; cell-surface TGF-beta-1 binds it on microvilli, a real but non-core non-canonical interaction distinct from the core receptor/SMAD signaling. Supporting Evidence: PMID:19366691 bound cell surface hyaluronidase Hyal-2 on microvilli |
| GO:0021915 neural tube development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: neural tube development. Reason: neural tube development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0021915 neural tube development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: neural tube development. Reason: neural tube development is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0030141 secretory granule | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: secretory granule. Reason: TGF-beta-1 is stored as the latent complex in secretory granules (including platelet alpha-granules) prior to regulated release; a genuine but non-core storage compartment of the secreted cytokine. Electronic transfer from the rat ortholog, consistent with this storage biology. |
| GO:0030154 cell differentiation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: cell differentiation. Reason: cell differentiation is a phylogenetic (PAINT) inference propagated across the TGF-beta ligand family (IBA, GO_REF:0000033). TGF-beta-1 directs this differentiation program through receptor-driven SMAD signaling in target cells; a genuine but downstream, context-dependent role of the secreted cytokine rather than a core molecular activity. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0030214 hyaluronan catabolic process | IDA PMID:17324121 Growth factor regulation of hyaluronan synthesis and degrada... | KEEP AS NON CORE | Summary: hyaluronan catabolic process. Reason: Annotates TGF-beta-1 to hyaluronan catabolic process. In human dermal fibroblasts TGF-beta-1 did not stimulate hyaluronan synthesis but increased hyaluronidase (HYAL) activity, favoring hyaluronan degradation. Modulating HYAL activity is a downstream transcriptional/enzymatic output of TGF-beta-1 receptor/SMAD signaling in fibroblasts, so the catabolic role is non-core to the ligand's core function. Supporting Evidence: PMID:17324121 but increased the activity of HYALs |
| GO:0030308 negative regulation of cell growth | IDA PMID:15334054 Hepatitis C viral proteins interact with Smad3 and different... | KEEP AS NON CORE | Summary: negative regulation of cell growth. Reason: Annotates TGF-beta-1 to negative regulation of cell growth. The paper frames TGF-beta/Smad3 signaling as mediating growth inhibition that HCV proteins antagonize. This antiproliferative/growth-inhibitory output is a downstream effect of TGF-beta-1 engaging its receptors and activating Smad3-dependent transcription, not the ligand's intrinsic receptor-binding activity, so it is peripheral (non-core) to the core function. Supporting Evidence: PMID:15334054 TGF-beta/Smad3-mediated transactivation and growth inhibition |
| GO:0030308 negative regulation of cell growth | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of cell growth. Reason: negative regulation of cell growth is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0030334 regulation of cell migration | TAS PMID:19018011 Holding their own: the noncanonical roles of Smad proteins. | KEEP AS NON CORE | Summary: regulation of cell migration. Reason: GO:0030334 regulation of cell migration is a TAS annotation placing TGF-beta-1-driven migration as a cellular output of canonical/non-canonical SMAD signaling. Migration control is a downstream consequence of receptor binding, hence non-core. This cited review concerns the non-canonical roles of Smad proteins (cell-cell adhesion, miRNA processing) and does not substantiate a cell-migration claim in the cached abstract, so the specific support rests on the author-stated (TAS) source text. |
| GO:0030335 positive regulation of cell migration | IDA PMID:19736306 Endoglin phosphorylation by ALK2 contributes to the regulati... | KEEP AS NON CORE | Summary: positive regulation of cell migration. Reason: GO:0030335 positive regulation of cell migration. In PC3/PC3-M prostate cancer cells, TGF-beta1 stimulates cell migration via ALK5/Smad2/3 and additionally neutralizes endoglin's anti-migratory effect by triggering ALK2/ALK5-mediated phosphorylation of the endoglin cytosolic domain, so TGF-beta1 promotes migration of these cells. This pro-migratory effect is a downstream, cell-context-specific (metastatic carcinoma) consequence of TGF-beta1 receptor engagement and its canonical/non-canonical signaling, not a core molecular activity the secreted ligand itself executes; non-core. Supporting Evidence: PMID:19736306 TGF-Ξ²1 stimulates cell migration via ALK5/Smad2 and 3 |
| GO:0030335 positive regulation of cell migration | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: positive regulation of cell migration. Reason: positive regulation of cell migration is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0030335 positive regulation of cell migration | IMP PMID:26169693 miR-208-3p promotes hepatocellular carcinoma cell proliferat... | KEEP AS NON CORE | Summary: positive regulation of cell migration. Reason: Positive regulation of cell migration is annotated from HCC invasion assays: depleting TGF-beta1 inhibited HCC cell invasion (transwell/Matrigel, a migration-dependent process), an effect reversed by miR-208-3p overexpression. The assay measures invasion rather than migration per se, and TGF-beta1 acts indirectly via the miR-208-3p/ARID2 axis, making this a downstream, cancer-context consequence of TGF-beta signaling rather than a core molecular function; kept non-core. Supporting Evidence: PMID:26169693 depeted TGFΞ²1 inhibited HCC cell invasion and colony formation ability |
| GO:0030424 axon | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: axon. Reason: Electronic transfer from the rat ortholog with no direct human evidence or supporting mechanism; axonal localization is not an established location for the secreted cytokine and is an over-annotation. |
| GO:0031012 extracellular matrix | HDA PMID:23979707 SILAC-based proteomics of human primary endothelial cell mor... | KEEP AS NON CORE | Summary: extracellular matrix. Reason: Latent TGF-beta-1 is deposited and stored in the extracellular matrix via LTBP and the latency-associated peptide, forming the sequestered reservoir from which integrin-mediated force releases the active cytokine; a genuine but non-core storage location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt during storage in extracellular matrix |
| GO:0031012 extracellular matrix | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: extracellular matrix. Reason: Latent TGF-beta-1 is deposited and stored in the extracellular matrix via LTBP and the latency-associated peptide, forming the sequestered reservoir from which integrin-mediated force releases the active cytokine; a genuine but non-core storage location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt during storage in extracellular matrix |
| GO:0031012 extracellular matrix | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: extracellular matrix. Reason: Latent TGF-beta-1 is deposited and stored in the extracellular matrix via LTBP and the latency-associated peptide, forming the sequestered reservoir from which integrin-mediated force releases the active cytokine; a genuine but non-core storage location. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt during storage in extracellular matrix |
| GO:0031093 platelet alpha granule lumen | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: platelet alpha granule lumen. Reason: Platelets are a major reservoir of TGF-beta-1, stored as the latent complex in the alpha-granule lumen and released on platelet degranulation; a genuine but non-core storage location of the secreted cytokine. |
| GO:0031093 platelet alpha granule lumen | TAS Reactome:R-HSA-481007 | KEEP AS NON CORE | Summary: platelet alpha granule lumen. Reason: Platelets are a major reservoir of TGF-beta-1, stored as the latent complex in the alpha-granule lumen and released on platelet degranulation; a genuine but non-core storage location of the secreted cytokine. |
| GO:0031100 animal organ regeneration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: animal organ regeneration. Reason: animal organ regeneration is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0031293 membrane protein intracellular domain proteolysis | IDA PMID:25310401 Sustained induction of collagen synthesis by TGF-Ξ² requires ... | KEEP AS NON CORE | Summary: membrane protein intracellular domain proteolysis. Reason: Membrane protein intracellular domain proteolysis refers to TGF-beta-1 triggering regulated intramembrane proteolysis (RIP) of the membrane-bound transcription factor CREB3L1, releasing its cytosolic domain. Importantly TGF-beta-1 does not perform the cleavage itself (S1P/S2P do); it induces RIP indirectly by repressing TM4SF20 through an ERK-dependent pathway. This is a highly indirect downstream effect of TGF-beta signaling on another protein's processing, clearly non-core for the ligand. Supporting Evidence: PMID:25310401 we determine that TGF-Ξ² stimulates RIP of CREB3L1 |
| GO:0031334 positive regulation of protein-containing complex assembly | IDA PMID:19366691 Transforming growth factor beta1 signaling via interaction w... | KEEP AS NON CORE | Summary: positive regulation of protein-containing complex assembly. Reason: TGF-beta-1 binding Hyal-2 drives recruitment of WOX1 and assembly of Hyal-2-WOX1 complexes; a real but non-core non-canonical branch of TGF-beta-1 action. Supporting Evidence: PMID:19366691 recruitment of proapoptotic WOX1 (also named WWOX or FOR) and formation of Hyal-2 |
| GO:0031536 positive regulation of exit from mitosis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of exit from mitosis. Reason: positive regulation of exit from mitosis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032355 response to estradiol | IDA PMID:18039789 Opposite regulation of transforming growth factors-beta2 and... | KEEP AS NON CORE | Summary: response to estradiol. Reason: GO:0032355 response to estradiol. PMID:18039789 studies regulation of endometrial TGF-beta isoforms by ovarian steroids but foregrounds TGF-beta2 and -beta3; TGF-beta1 is noted mainly for its cycle timing (maximal at menstruation). A response-to-estradiol relationship for TGF-beta1 is a tissue-specific regulatory input, not a core activity. The abstract does not separate an estradiol-specific response of TGF-beta1, so this annotation rests on the curator's full-text reading (not cached). |
| GO:0032355 response to estradiol | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to estradiol. Reason: response to estradiol is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of estradiol; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032570 response to progesterone | IDA PMID:18039789 Opposite regulation of transforming growth factors-beta2 and... | KEEP AS NON CORE | Summary: response to progesterone. Reason: GO:0032570 response to progesterone. In PMID:18039789 ovarian steroids regulate endometrial TGF-beta isoform expression and TGF-betas are reported to mediate progesterone's repression of matrix metalloproteinases; the demonstrated progesterone regulation in the abstract concerns TGF-beta2/-beta3 rather than TGF-beta1 specifically. A progesterone-response relationship for TGF-beta1 is a context-specific regulatory input rather than a core function, and the TGF-beta1-specific claim rests on the curator's full-text reading (not cached). |
| GO:0032570 response to progesterone | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: response to progesterone. Reason: response to progesterone is an electronic (IEA) annotation under GO_REF:0000117. this term records that TGF-beta-1 expression or activity is modulated in the context of progesterone; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032667 regulation of interleukin-23 production | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: regulation of interleukin-23 production. Reason: regulation of interleukin-23 production is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032700 negative regulation of interleukin-17 production | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of interleukin-17 production. Reason: negative regulation of interleukin-17 production is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032740 positive regulation of interleukin-17 production | IDA PMID:18453574 Activation of a TGF-beta-specific multistep gene expression ... | KEEP AS NON CORE | Summary: positive regulation of interleukin-17 production. Reason: Annotates TGF-beta-1 to positive regulation of interleukin-17 production (IDA). The abstract shows TGF-beta-1 (with IL-4/glucocorticoid) induces a macrophage gene program that upregulates IL-17 receptor B (IL17RB), but it describes the receptor rather than IL-17 cytokine production itself. Any effect on IL-17 production is a downstream immunomodulatory output of TGF-beta-1 receptor/SMAD signaling and non-core; the abstract does not verbatim substantiate IL-17 production, so the claim rests on the uncached full text and no quote is asserted. |
| GO:0032740 positive regulation of interleukin-17 production | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of interleukin-17 production. Reason: positive regulation of interleukin-17 production is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032755 positive regulation of interleukin-6 production | IMP PMID:25196641 Inhibition of TGF-Ξ²/SMAD3/NF-ΞΊB signaling by microRNA-491 is... | KEEP AS NON CORE | Summary: positive regulation of interleukin-6 production. Reason: GO:0032755 positive regulation of interleukin-6 production. PMID:25196641 shows that in hepatocellular carcinoma cells the TGF-beta/Smad3 axis drives NF-kappaB/IL-6/STAT-3 signaling, and that suppressing Smad3 inactivates this IL-6 arm, placing TGF-beta1 upstream of IL-6 output in this cancer context. This is a downstream, context-specific consequence of Smad3 signaling (the abstract names IL-6 at the pathway level), not a core molecular activity. Supporting Evidence: PMID:25196641 decreased the expression/function of SMAD3, leading to the inactivation of NF-ΞΊB/IL-6/STAT-3 signaling |
| GO:0032755 positive regulation of interleukin-6 production | IMP PMID:32141990 miR-4286/TGF-Ξ²1/Smad3-Negative Feedback Loop Ameliorated Vas... | KEEP AS NON CORE | Summary: positive regulation of interleukin-6 production. Reason: GO:0032755 positive regulation of interleukin-6 production. In the ox-LDL/atherosclerosis HUVEC model of PMID:32141990, silencing TGF-beta1 reversed the ox-LDL-induced inflammatory response, placing TGF-beta1 upstream of the endothelial pro-inflammatory cytokine program of which IL-6 is one component. This is a context-specific, downstream consequence of TGF-beta1 receptor engagement and Smad3 signaling, not a core molecular activity. The cited abstract documents a general inflammatory response but does not name IL-6 specifically, so the IL-6-specific claim rests on the curator's reading of the full text (not cached). |
| GO:0032760 positive regulation of tumor necrosis factor production | IMP PMID:32141990 miR-4286/TGF-Ξ²1/Smad3-Negative Feedback Loop Ameliorated Vas... | KEEP AS NON CORE | Summary: positive regulation of tumor necrosis factor production. Reason: GO:0032760 positive regulation of tumor necrosis factor production. As with the IL-6 row, this reflects TGF-beta1 driving the ox-LDL-induced endothelial inflammatory program in PMID:32141990; TNF is one cytokine in that response. It is a downstream, vascular-injury-context output of receptor binding plus Smad3 signaling rather than a core activity. The cached abstract refers only to a general inflammatory response and does not mention TNF, so the TNF-specific claim rests on the curator's full-text reading (not cached). |
| GO:0032801 receptor catabolic process | IDA PMID:17878231 Cholesterol suppresses cellular TGF-beta responsiveness: imp... | KEEP AS NON CORE | Summary: receptor catabolic process. Reason: GO:0032801 receptor catabolic process relates to this study's finding that cholesterol loading drives TGF-beta receptors into lipid rafts/caveolae and promotes rapid degradation, thereby suppressing TGF-beta responsiveness. The process is about turnover/degradation of the TGF-beta receptor system, a regulatory event imposed on the pathway (and on the ligand) rather than a catalytic or binding function that TGFB1 itself performs; the abstract describes degradation in the atherogenesis context but does not substantiate TGFB1 executing receptor catabolism, so this is a peripheral, context-specific annotation kept as non-core (no abstract sentence directly supports the term; the detail rests on the uncached full text). |
| GO:0032930 positive regulation of superoxide anion generation | IDA PMID:22073128 Poly(ADP-ribose) polymerase 1 is indispensable for transform... | KEEP AS NON CORE | Summary: positive regulation of superoxide anion generation. Reason: GO:0032930 positive regulation of superoxide anion generation. In rat vascular smooth muscle cells TGF-Ξ²1 promoted reactive oxygen species generation, which in turn activated PARP1 upstream of Smad3; the induced ROS is an early signaling intermediate of TGFB1 action, not a molecular activity of the ligand, so the annotation is a downstream, non-core consequence. Note that the paper documents ROS generically (measured by DCFH2-DA) rather than superoxide anion specifically, so the term is more precise than what was actually assayed. Supporting Evidence: PMID:22073128 TGF-Ξ²1 treatment promoted ROS generation in VSMCs |
| GO:0032967 positive regulation of collagen biosynthetic process | IDA PMID:19734317 Mesenchymal stem cells produce Wnt isoforms and TGF-beta1 th... | KEEP AS NON CORE | Summary: positive regulation of collagen biosynthetic process. Reason: GO:0032967 positive regulation of collagen biosynthetic process. MSC-derived, acid-activated TGF-Ξ²1 upregulated Ξ±1-procollagen (COL1A1) gene expression in lung fibroblast target cells, and anti-TGF-Ξ² antibody blocked this collagen induction, establishing TGF-Ξ²1 as the factor driving collagen biosynthesis. This stimulation of collagen gene expression is a downstream SMAD-dependent transcriptional consequence in the target fibroblast rather than a core molecular activity of the ligand, so it is non-core. Supporting Evidence: PMID:19734317 Addition of anti-TGF-Ξ² to the MSC-CM blocked upregulation of collagen gene expression |
| GO:0032967 positive regulation of collagen biosynthetic process | IDA PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: positive regulation of collagen biosynthetic process. Reason: Positive regulation of collagen biosynthetic process is directly supported: TGF-beta1 increased collagen synthesis in treated human aortic fibroblasts (IDA). Stimulating collagen production is a classic profibrotic effect downstream of TGFBR binding and SMAD-driven transcription of matrix genes, i.e. a biological-process output rather than the ligand's core receptor-binding/signal-initiating activity, so it is retained as non-core. Supporting Evidence: PMID:22269326 Collagen synthesis was increased in TGF-Ξ²1βtreated cells compared with that in an untreated control group. |
| GO:0032967 positive regulation of collagen biosynthetic process | IDA PMID:25310401 Sustained induction of collagen synthesis by TGF-Ξ² requires ... | KEEP AS NON CORE | Summary: positive regulation of collagen biosynthetic process. Reason: Positive regulation of collagen biosynthetic process is well supported: TGF-beta-1 activates COL1A1 synthesis, acutely via SMAD2/3-SMAD4 and in a sustained manner via CREB3L1-driven transcription of collagen-ECM genes. Stimulating collagen production is a canonical downstream transcriptional output of TGFBR binding and SMAD signaling, a biological process rather than the ligand's core molecular activity, so it is kept as non-core. Supporting Evidence: PMID:25310401 Transforming growth factor-Ξ² (TGF-Ξ²), a cytokine homologous to BMP2, also activates COL1A1 synthesis |
| GO:0032967 positive regulation of collagen biosynthetic process | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: positive regulation of collagen biosynthetic process. Reason: positive regulation of collagen biosynthetic process is an electronic (IEA) annotation under GO_REF:0000120. TGF-beta-1 is a strong driver of matrix deposition, but the biosynthetic/assembly steps are performed by collagen and ECM machinery in responding cells; for the ligand this is a downstream SMAD-dependent transcriptional consequence rather than a core activity. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0032967 positive regulation of collagen biosynthetic process | IGI PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: positive regulation of collagen biosynthetic process. Reason: Genetic-interaction evidence that TGF-beta-1 promotes collagen production in the aortic-fibroblast/miR-29b system, consistent with and reinforcing the IDA row 282. Enhancing collagen biosynthesis is a downstream profibrotic consequence of canonical TGF-beta signaling in this vascular context, not a core molecular function, so non-core is correct. Supporting Evidence: PMID:22269326 Collagen synthesis was increased in TGF-Ξ²1βtreated cells compared with that in an untreated control group. |
| GO:0032967 positive regulation of collagen biosynthetic process | IMP PMID:11158066 Human leiomyoma smooth muscle cells show increased expressio... | KEEP AS NON CORE | Summary: positive regulation of collagen biosynthetic process. Reason: Annotates TGF-beta-1 to positive regulation of collagen biosynthetic process (IMP). Neutralizing endogenous TGF-betas reduced type I and type III collagen mRNA by 45-60% in myometrial/leiomyoma cells, indicating TGF-beta-1 supports collagen production. This pro-fibrotic transcriptional output is a classic downstream effect of TGF-beta-1-SMAD signaling on matrix genes, so it is non-core relative to the ligand's receptor-binding activity. Supporting Evidence: PMID:11158066 endogenous TGF betas are important for collagen production |
| GO:0033280 response to vitamin D | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to vitamin D. Reason: response to vitamin D is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of vitamin D; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0034125 negative regulation of MyD88-dependent toll-like receptor signaling pathway | IDA PMID:21897371 Smad6-specific recruitment of Smurf E3 ligases mediates TGF-... | KEEP AS NON CORE | Summary: negative regulation of MyD88-dependent toll-like receptor signaling pathway. Reason: GO:0034125 negative regulation of MyD88-dependent toll-like receptor signaling pathway is directly supported: TGF-beta-1 drives Smad6/Smurf-mediated K48 polyubiquitination and degradation of MyD88, suppressing MyD88-dependent TLR4/TLR2 pro-inflammatory signaling. This anti-inflammatory effect is a downstream consequence of TGFBR/SMAD signaling acting on the TLR adaptor, so it is a non-core immunomodulatory role relative to the core receptor-binding function. Supporting Evidence: PMID:21897371 TGF-Ξ²1-mediated negative regulation of MyD88-dependent pro-inflammatory signalling |
| GO:0034616 response to laminar fluid shear stress | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to laminar fluid shear stress. Reason: response to laminar fluid shear stress is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of laminar fluid shear stress; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0034713 type I transforming growth factor beta receptor binding | IMP PMID:8167376 Cloning and developmental expression of the chick type II an... | ACCEPT | Summary: Type I TGF-beta receptor binding. Reason: Core receptor-binding function. |
| GO:0034713 type I transforming growth factor beta receptor binding | IPI PMID:10885742 Activin receptor-like kinase 2 can mediate atrioventricular ... | ACCEPT | Summary: Type I TGF-beta receptor binding. Reason: Core receptor-binding function. |
| GO:0034714 type III transforming growth factor beta receptor binding | IEA GO_REF:0000117 | ACCEPT | Summary: Type III TGF-beta receptor binding. Reason: Core receptor-binding function (betaglycan). |
| GO:0034714 type III transforming growth factor beta receptor binding | IMP PMID:8167376 Cloning and developmental expression of the chick type II an... | ACCEPT | Summary: Type III TGF-beta receptor binding. Reason: Core receptor-binding function (betaglycan). |
| GO:0034714 type III transforming growth factor beta receptor binding | IPI PMID:10092230 Requirement of type III TGF-beta receptor for endocardial ce... | ACCEPT | Summary: Type III TGF-beta receptor binding. Reason: Core receptor-binding function (betaglycan). |
| GO:0035902 response to immobilization stress | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to immobilization stress. Reason: response to immobilization stress is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of immobilization stress; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0036120 cellular response to platelet-derived growth factor stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to platelet-derived growth factor stimulus. Reason: cellular response to platelet-derived growth factor stimulus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of platelet-derived growth factor stimulus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0036446 myofibroblast differentiation | NAS PMID:28095798 miR-27b inhibits fibroblast activation via targeting TGFΞ² si... | KEEP AS NON CORE | Summary: myofibroblast differentiation. Reason: GO:0036446 myofibroblast differentiation. In human lung fibroblasts TGF-Ξ²1 increased Ξ±-smooth muscle actin (the defining myofibroblast marker) together with collagens and enhanced contractility, i.e. it drove fibroblast-to-myofibroblast activation (the paper shows miR-27b opposes this by targeting TGFBR1/SMAD2). Myofibroblast differentiation is a downstream SMAD-dependent transcriptional/phenotypic program in the responding fibroblast, not a molecular activity of the secreted ligand, so it is non-core. Supporting Evidence: PMID:28095798 mRNA expression of COL1A1, COL3A1, COL4A1 and Ξ±-SMA was increased by TGFΞ²1 treatment |
| GO:0042127 regulation of cell population proliferation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: regulation of cell population proliferation. Reason: regulation of cell population proliferation is a phylogenetic (PAINT) inference propagated across the TGF-beta ligand family (IBA, GO_REF:0000033). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0042306 regulation of protein import into nucleus | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: regulation of protein import into nucleus. Reason: regulation of protein import into nucleus is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 influences the nuclear import of downstream effectors (such as activated SMAD complexes) indirectly through receptor binding and signaling in responding cells, rather than performing nuclear transport itself; retained as a genuine but non-core regulatory consequence. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0042307 positive regulation of protein import into nucleus | IDA PMID:19366691 Transforming growth factor beta1 signaling via interaction w... | KEEP AS NON CORE | Summary: positive regulation of protein import into nucleus. Reason: The Hyal-2-WOX1 complex formed on TGF-beta-1 engagement of cell-surface Hyal-2 relocates to the nucleus; a real but non-core non-canonical branch distinct from the core receptor/SMAD signaling. Supporting Evidence: PMID:19366691 for relocation to the nuclei |
| GO:0042475 odontogenesis of dentin-containing tooth | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: odontogenesis of dentin-containing tooth. Reason: odontogenesis of dentin-containing tooth is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0042552 myelination | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: myelination. Reason: myelination is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0042802 identical protein binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: identical protein binding. Reason: TGF-beta-1 is a disulfide-linked homodimer, and this identical protein binding is that self-association; a real structural property of the cytokine rather than its core receptor-binding/SMAD-signaling molecular function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Homodimer; disulfide-linked |
| GO:0042802 identical protein binding | IPI PMID:21677751 Latent TGF-Ξ² structure and activation. | KEEP AS NON CORE | Summary: identical protein binding. Reason: TGF-beta-1 is a disulfide-linked homodimer, and this identical protein binding is that self-association; a real structural property of the cytokine rather than its core receptor-binding/SMAD-signaling molecular function. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt Homodimer; disulfide-linked |
| GO:0043025 neuronal cell body | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: neuronal cell body. Reason: Electronic transfer from the rat ortholog; reflects neuronal expression of the producing cells rather than an established functional location of the secreted protein, so it is an over-annotation as a cellular component. |
| GO:0043065 positive regulation of apoptotic process | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of apoptotic process. Reason: positive regulation of apoptotic process is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0043117 positive regulation of vascular permeability | IDA PMID:21168935 Tyrosine phosphorylation of VE-cadherin and claudin-5 is ass... | KEEP AS NON CORE | Summary: positive regulation of vascular permeability. Reason: Annotates TGF-beta-1 to positive regulation of vascular permeability. The paper shows TGF-beta-1 produces a dose-dependent increase in paracellular permeability of CNS-derived endothelial monolayers. Increased vascular permeability is a downstream physiological effect of TGF-beta-1 receptor signaling acting on endothelial junctions, so it is non-core relative to the ligand's receptor-binding activity. Supporting Evidence: PMID:21168935 TGF-Ξ²1 caused a dose-dependent increase in paracellular permeability |
| GO:0043123 positive regulation of canonical NF-kappaB signal transduction | IMP PMID:25196641 Inhibition of TGF-Ξ²/SMAD3/NF-ΞΊB signaling by microRNA-491 is... | KEEP AS NON CORE | Summary: positive regulation of canonical NF-kappaB signal transduction. Reason: GO:0043123 positive regulation of canonical NF-kappaB signal transduction. PMID:25196641 shows the TGF-beta/Smad3 pathway drives NF-kappaB signaling in hepatocellular carcinoma cells, with Smad3 knockdown inactivating the NF-kappaB/IL-6/STAT-3 axis. NF-kappaB activation is a downstream, non-canonical cross-talk branch of TGF-beta1 receptor/Smad signaling in this tumor context, not a core activity. Supporting Evidence: PMID:25196641 decreased the expression/function of SMAD3, leading to the inactivation of NF-ΞΊB/IL-6/STAT-3 signaling |
| GO:0043410 positive regulation of MAPK cascade | IDA PMID:26572508 Rotavirus-induced miR-142-5p elicits proviral milieu by targ... | KEEP AS NON CORE | Summary: positive regulation of MAPK cascade. Reason: GO:0043410 positive regulation of MAPK cascade reflects TGF-beta-1 engaging non-canonical (SMAD-independent) signaling, of which MAPK branches are a part, in rotavirus-infected cells. The abstract names non-canonical TGFbeta signalling and apoptosis but does not explicitly identify a MAPK cascade, so the specific MAPK-activation claim rests on the uncited full text. As a non-canonical branch downstream of receptor binding it is a non-core consequence of the core function. |
| GO:0043536 positive regulation of blood vessel endothelial cell migration | IDA PMID:18555217 Differential involvement of TGF-beta1 in mediating the motog... | KEEP AS NON CORE | Summary: positive regulation of blood vessel endothelial cell migration. Reason: GO:0043536 positive regulation of blood vessel endothelial cell migration reflects the stimulatory arm of TGF-beta1's biphasic effect on endothelial migration (stimulation at low concentrations), shown to mediate the promigratory action of thrombospondin-1 on endothelial cells. This is an angiogenesis-related consequence of TGF-beta1 receptor engagement and SMAD signaling in endothelium rather than the core ligand-receptor binding activity, so it is non-core. Supporting Evidence: PMID:18555217 the effects of TSP-1 on endothelial cell migration are mediated by TGF-beta1 |
| GO:0043537 negative regulation of blood vessel endothelial cell migration | IDA PMID:18555217 Differential involvement of TGF-beta1 in mediating the motog... | KEEP AS NON CORE | Summary: negative regulation of blood vessel endothelial cell migration. Reason: GO:0043537 negative regulation of blood vessel endothelial cell migration captures the inhibitory arm of TGF-beta1's biphasic, concentration-dependent effect on endothelial migration (inhibition at high concentrations), again mediating the corresponding effect of thrombospondin-1. The same cytokine thus both promotes and restrains endothelial migration depending on dose; both are downstream endothelial responses to receptor binding and SMAD signaling, not the core activity, and are appropriately non-core. Supporting Evidence: PMID:18555217 the effects of TSP-1 on endothelial cell migration are mediated by TGF-beta1 |
| GO:0043539 protein serine/threonine kinase activator activity | IEA GO_REF:0000107 | ACCEPT | Summary: Protein serine/threonine kinase activator activity - activates the TGF-beta receptor kinase. Reason: Core: ligand binding activates the receptor Ser/Thr kinase. |
| GO:0044877 protein-containing complex binding | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: protein-containing complex binding. Reason: As a binding MF this records TGF-beta-1's association with protein-containing complexes, chiefly the latency-associated-peptide/LTBP latent complex and the GARP-presented latent form; a real but non-core molecular interaction rather than the core receptor-binding/SMAD-signaling activity. Supporting Evidence: file:human/TGFB1/TGFB1-uniprot.txt interaction is non-covalent and maintains TGF-beta-1 in a latent state |
| GO:0045066 regulatory T cell differentiation | IDA PMID:32644293 The deubiquitinase USP44 promotes Treg function during infla... | KEEP AS NON CORE | Summary: regulatory T cell differentiation. Reason: GO:0045066 regulatory T cell differentiation. TGF-beta1 (with IL-2) is the canonical cytokine driving induced Treg (iTreg) differentiation; in this paper TGF-beta/Smad3 signaling transcriptionally induces the deubiquitinase USP44, which stabilizes FOXP3 and is required for Treg function. The role in Treg differentiation is a downstream transcriptional/lineage program set in motion by TGF-beta1 receptor binding and SMAD signaling in a specific (immune) cell context, not a distinct core molecular activity of the ligand; non-core. Supporting Evidence: PMID:32644293 Notably, TGF-Ξ² induces USP44 expression during iTreg differentiation |
| GO:0045216 cell-cell junction organization | IDA PMID:18505915 Transforming growth factor-beta1, transforming growth factor... | KEEP AS NON CORE | Summary: cell-cell junction organization. Reason: GO:0045216 cell-cell junction organization reflects TGF-beta-1-induced loss of cell-cell junctions and E-cadherin downregulation as part of the EMT program in ovarian cancer cells. Junction disassembly is a downstream SMAD3-dependent effect of receptor engagement, not a direct activity of the ligand, so it is kept as non-core; it is the junctional component of the EMT response rather than a separate core function. Supporting Evidence: PMID:18505915 loss of cell-cell junctions |
| GO:0045216 cell-cell junction organization | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: cell-cell junction organization. Reason: cell-cell junction organization is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0045471 response to ethanol | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to ethanol. Reason: response to ethanol is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of ethanol; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0045591 positive regulation of regulatory T cell differentiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of regulatory T cell differentiation. Reason: positive regulation of regulatory T cell differentiation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0045596 negative regulation of cell differentiation | IEP PMID:19357233 Myostatin reduces Akt/TORC1/p70S6K signaling, inhibiting myo... | KEEP AS NON CORE | Summary: negative regulation of cell differentiation. Reason: Annotates TGF-beta-1 to negative regulation of cell differentiation (IEP). The paper notes that TGF-beta-family molecules, explicitly including TGF-beta-1, can block (myoblast) differentiation via activin receptor/Smad2/3 signaling. Inhibition of differentiation is a downstream transcriptional consequence of TGF-beta-1 receptor/SMAD signaling in a specific lineage, so it is non-core relative to the ligand's receptor-binding activity. Supporting Evidence: PMID:19357233 can also block differentiation, including TGF-beta(1) |
| GO:0045597 positive regulation of cell differentiation | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: positive regulation of cell differentiation. Reason: positive regulation of cell differentiation is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 directs this differentiation program through receptor-driven SMAD signaling in target cells; a genuine but downstream, context-dependent role of the secreted cytokine rather than a core molecular activity. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0045599 negative regulation of fat cell differentiation | IDA PMID:15040835 Cooperation between TGF-beta and Wnt pathways during chondro... | KEEP AS NON CORE | Summary: negative regulation of fat cell differentiation. Reason: GO:0045599 negative regulation of fat cell differentiation reflects TGF-beta1 suppressing adipocyte differentiation of human marrow stromal cells (repression of lipoprotein lipase) at the same time it promotes chondrogenesis. This is a mesenchymal lineage-choice consequence of TGF-beta1/SMAD signaling, context-specific and downstream of the core receptor interaction, hence non-core. Supporting Evidence: PMID:15040835 TGF-beta stimulated chondrocyte differentiation and inhibited adipocyte differentiation of hMSCs in vitro |
| GO:0045662 negative regulation of myoblast differentiation | IDA PMID:9770491 Inhibition of myogenesis by transforming growth factor beta ... | KEEP AS NON CORE | Summary: negative regulation of myoblast differentiation. Reason: GO:0045662 negative regulation of myoblast differentiation. The paper shows TGF-Ξ² (5 ng/mL TGF-Ξ²1) reversibly inhibits terminal differentiation of myogenic cells (in a density-dependent manner) by triggering nuclear export of the transcription factor MEF2. Inhibition of myoblast differentiation is a downstream, context-dependent consequence of TGFB1 receptor signaling acting on the myogenic transcriptional machinery, not a core molecular activity of the ligand, so it is non-core. Supporting Evidence: PMID:9770491 inhibit differentiation of myogenic cells only when they were grown to high density |
| GO:0045742 positive regulation of epidermal growth factor receptor signaling pathway | IDA PMID:18625725 Transforming growth factor beta engages TACE and ErbB3 to ac... | KEEP AS NON CORE | Summary: positive regulation of epidermal growth factor receptor signaling pathway. Reason: GO:0045742 positive regulation of epidermal growth factor receptor signaling pathway. PMID:18625725 shows TGF-beta triggers TACE/ADAM17-mediated shedding of ErbB/EGFR ligands (TGF-alpha, amphiregulin, heregulin) that then transactivate ErbB receptor signaling. TGF-beta1's effect on EGFR signaling is thus an indirect cross-talk consequence of its receptor/Smad signaling, downstream and cell-context-specific, not a core activity. Supporting Evidence: PMID:18625725 induced phosphorylation of TACE/ADAM17 and its translocation to the cell surface, resulting in increased secretion of TGF-alpha, amphiregulin, and heregulin. |
| GO:0045786 negative regulation of cell cycle | IDA PMID:11502704 Altered growth responses of pulmonary artery smooth muscle c... | KEEP AS NON CORE | Summary: negative regulation of cell cycle. Reason: GO:0045786 negative regulation of cell cycle captures the classic cytostatic action of TGF-beta1, here shown as inhibition of basal and serum-stimulated DNA synthesis and proliferation in control pulmonary artery smooth muscle cells. This antiproliferative/growth-arrest response is a downstream consequence of TGF-beta1 receptor binding and SMAD signaling; although important biologically (and reversed to a growth-stimulatory response in pulmonary-hypertension cells), it is a cellular output peripheral to the core ligand-receptor function, so it is non-core. Supporting Evidence: PMID:11502704 inhibited the proliferation of serum-stimulated PASMCs |
| GO:0045892 negative regulation of DNA-templated transcription | IDA PMID:15702480 Interaction and functional interplay between endoglin and AL... | KEEP AS NON CORE | Summary: negative regulation of DNA-templated transcription. Reason: Annotates TGF-beta-1 to negative regulation of DNA-templated transcription (IDA). The cited paper characterizes the endoglin-ALK1 endothelial TGF-beta receptor complex and its modulation of TGF-beta/ALK1 vs ALK5 signaling; the abstract does not itself report a specific negative transcriptional effect of TGF-beta-1. Transcriptional repression of target genes is a downstream, promoter-specific Smad output of receptor signaling and thus non-core; the specific negative-regulation claim rests on the uncached full-text reporter data, so no verbatim quote is asserted. |
| GO:0045892 negative regulation of DNA-templated transcription | IDA PMID:18832382 HMGA2 and Smads co-regulate SNAIL1 expression during inducti... | KEEP AS NON CORE | Summary: negative regulation of DNA-templated transcription. Reason: GO:0045892 negative regulation of DNA-templated transcription most plausibly refers to repression of E-cadherin (and other epithelial genes) during TGF-beta1-induced EMT, achieved indirectly through SMAD/HMGA2-driven induction of the transcriptional repressor SNAIL1. The abstract documents positive regulation of SNAIL1 and that SNAIL1 is an E-cadherin repressor, but contains no sentence in which TGF-beta1 itself directly negatively regulates transcription of a specific target; that mechanism rests on the uncached full text. The term is a downstream, indirect transcriptional consequence of receptor binding and SMAD signaling and is retained as non-core. |
| GO:0045893 positive regulation of DNA-templated transcription | IDA PMID:14517293 Myostatin signals through a transforming growth factor beta-... | KEEP AS NON CORE | Summary: positive regulation of DNA-templated transcription. Reason: GO:0045893 positive regulation of DNA-templated transcription. This study (focused on myostatin) uses TGF-beta as the positive control and shows TGF-beta induces Smad2/3-responsive transcription, activating the 3TP-Lux, A3-Lux and SBE4-Lux luciferase reporters in HepG2 cells. Positive regulation of transcription is the general downstream nuclear readout of TGF-beta1-activated R-SMAD complexes rather than a molecular activity of the secreted ligand itself, and the term is far broader than the specific Smad2/3 target programs; non-core. Supporting Evidence: PMID:14517293 TGF-Ξ² treatment of HepG2 cells induced luciferase activity from 3TP-Lux, A3-Lux, and SBE4-Lux |
| GO:0045893 positive regulation of DNA-templated transcription | IDA PMID:15334054 Hepatitis C viral proteins interact with Smad3 and different... | KEEP AS NON CORE | Summary: positive regulation of DNA-templated transcription. Reason: Annotates TGF-beta-1 to positive regulation of DNA-templated transcription. The paper demonstrates TGF-beta/Smad3-mediated transcriptional activation (e.g. of the p21 promoter) that HCV core and NS3 impair by blocking Smad3 DNA binding. Transcriptional activation here is executed by the nuclear Smad3 complex downstream of ligand-receptor binding; TGF-beta-1 itself is the extracellular trigger, so this is a non-core downstream readout of SMAD signaling. Supporting Evidence: PMID:15334054 TGF-beta/Smad3-mediated transcriptional activation |
| GO:0045893 positive regulation of DNA-templated transcription | IDA PMID:9389648 Dual role of the Smad4/DPC4 tumor suppressor in TGFbeta-indu... | KEEP AS NON CORE | Summary: positive regulation of DNA-templated transcription. Reason: GO:0045893 positive regulation of DNA-templated transcription. This paper dissects how TGF-beta-activated Smad2 carries Smad4 into the nucleus to form a Smad2/Smad4/FAST-1 complex that binds DNA (the Mix.2 ARE) and activates transcription of the A3CAT reporter. Transcriptional activation is the canonical but generic downstream output of TGF-beta1/SMAD signaling; the term describes a consequence of receptor-activated SMAD transcription factors acting in the nucleus, not the core receptor-binding activity of the ligand, so it is non-core. Supporting Evidence: PMID:9389648 Upon ligand binding, the receptors of the TGFΞ² family phosphorylate Smad proteins, which then move into the nucleus where they activate transcription |
| GO:0045893 positive regulation of DNA-templated transcription | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: positive regulation of DNA-templated transcription. Reason: positive regulation of DNA-templated transcription is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). this transcriptional/expression effect is the downstream output of TGF-beta-1 receptor binding and SMAD activation in responding cells, not an activity the ligand itself executes; retained as a genuine but non-core regulatory consequence. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:12574355 Human activation-induced cytidine deaminase is induced by IL... | KEEP AS NON CORE | Summary: positive regulation of transcription by RNA polymerase II. Reason: GO:0045944 positive regulation of transcription by RNA polymerase II. The cached abstract of PMID:12574355 concerns IL-4/CD40-driven induction of AID via JAK/STAT6 in B cells and does not mention TGF-beta1; TGF-beta is a well-known cofactor in B-cell isotype switching, so the transcription-activation annotation to TGFB1 likely rests on full-text data the curator read (not cached). Positive regulation of Pol II transcription is in any case a broad downstream SMAD-mediated effect rather than a core molecular activity. Per policy the experimental annotation is retained, not removed, despite the abstract foregrounding IL-4/AID. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:18832382 HMGA2 and Smads co-regulate SNAIL1 expression during inducti... | KEEP AS NON CORE | Summary: positive regulation of transcription by RNA polymerase II. Reason: GO:0045944 positive regulation of transcription by RNA polymerase II reflects TGF-beta1/SMAD transcriptional activation of the protein-coding gene SNAIL1, with the pathway cooperating with HMGA2 to increase SMAD occupancy at the SNAIL1 promoter and thereby raise SNAIL1 expression. This is a nuclear transcriptional output downstream of receptor engagement and SMAD translocation, peripheral to the core cytokine-receptor binding activity, so it is non-core. Supporting Evidence: PMID:18832382 an increased binding of Smads to the SNAIL1 promoter |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:22073128 Poly(ADP-ribose) polymerase 1 is indispensable for transform... | KEEP AS NON CORE | Summary: positive regulation of transcription by RNA polymerase II. Reason: GO:0045944 positive regulation of transcription by RNA polymerase II. In VSMCs TGF-Ξ²1 drove Smad3-dependent transactivation and upregulated transcription of target genes (collagen IΞ±1, collagen IIIΞ±1, TIMP1). This Pol II transcriptional activation is the canonical downstream nuclear output of the TGFB1/SMAD3 cascade executed by the SMAD transcription factors in the responding cell, not a molecular activity of the secreted ligand itself, so it is retained as non-core relative to TGFB1's core receptor-binding function. Supporting Evidence: PMID:22073128 TGF-Ξ²1 treatment resulted in up-regulation of mRNA levels of CoIΞ±1, CoIIIΞ±1, TIMP1 |
| GO:0048298 positive regulation of isotype switching to IgA isotypes | IDA PMID:14988498 Impaired IgA class switching in APRIL-deficient mice. | KEEP AS NON CORE | Summary: positive regulation of isotype switching to IgA isotypes. Reason: GO:0048298 positive regulation of isotype switching to IgA isotypes. The cached abstract of PMID:14988498 concerns APRIL's role in IgA class switching and does not mention TGF-beta1; however TGF-beta1 is the canonical switch factor directing IgA class-switch recombination, so this immunological role is well established and the TGF-beta1-specific evidence rests on the curator's full-text reading (not cached). It is a cell-type-specific downstream function of receptor/Smad signaling, non-core relative to receptor binding. The experimental annotation is retained, not removed, despite the abstract foregrounding APRIL. |
| GO:0048535 lymph node development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: lymph node development. Reason: lymph node development is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0048565 digestive tract development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: digestive tract development. Reason: digestive tract development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0048642 negative regulation of skeletal muscle tissue development | IDA PMID:9770491 Inhibition of myogenesis by transforming growth factor beta ... | KEEP AS NON CORE | Summary: negative regulation of skeletal muscle tissue development. Reason: GO:0048642 negative regulation of skeletal muscle tissue development. The same study establishes that TGF-Ξ² inhibits myogenesis through MEF2 relocalization from the nucleus to the cytoplasm, preventing MEF2 from participating in the active transcriptional complex needed for muscle-gene expression. Suppression of skeletal-muscle differentiation is a downstream developmental consequence of TGFB1 signaling in myogenic cells, not a direct molecular activity of the ligand, so it is retained as non-core. Supporting Evidence: PMID:9770491 the inhibition of myogenesis by TGF-Ξ² is mediated through MEF2 localization to the cytoplasm |
| GO:0048661 positive regulation of smooth muscle cell proliferation | IDA PMID:28467929 PPARΞ³ Links BMP2 and TGFΞ²1 Pathways in Vascular Smooth Muscl... | KEEP AS NON CORE | Summary: positive regulation of smooth muscle cell proliferation. Reason: Annotates TGF-beta-1 to positive regulation of smooth muscle cell proliferation. The paper identifies a pro-proliferative TGF-beta-1-Stat3-FoxO1 axis in vascular smooth muscle cells. Promotion of VSMC proliferation is a cell-type- and context-specific downstream output of the receptor-activated signaling axis, so it is non-core relative to TGF-beta-1's core receptor-binding/SMAD-initiating function. Supporting Evidence: PMID:28467929 pro-proliferative TGFΞ²1-Stat3-FoxO1 axis in VSMCs |
| GO:0048661 positive regulation of smooth muscle cell proliferation | IDA PMID:31023188 LRP1 Deficiency in Vascular SMC Leads to Pulmonary Arterial ... | KEEP AS NON CORE | Summary: positive regulation of smooth muscle cell proliferation. Reason: GO:0048661 positive regulation of smooth muscle cell proliferation is supported by TGF-beta-1-induced proliferation of pulmonary artery smooth muscle cells via the pSmad3-CTGF axis, enhanced when LRP1 is lost and implicated in pulmonary arterial hypertension remodeling. SMC proliferation is a downstream pathological output of canonical TGFBR/SMAD3 signaling, hence a non-core, context-specific consequence of the core receptor-binding function. Supporting Evidence: PMID:31023188 increased TGFΞ²1-induced PASMC proliferation that was prevented by pioglitazone |
| GO:0048839 inner ear development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: inner ear development. Reason: inner ear development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0050679 positive regulation of epithelial cell proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of epithelial cell proliferation. Reason: positive regulation of epithelial cell proliferation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0050680 negative regulation of epithelial cell proliferation | IDA PMID:9950587 Bone morphogenetic proteins and growth and differentiation f... | KEEP AS NON CORE | Summary: negative regulation of epithelial cell proliferation. Reason: GO:0050680 negative regulation of epithelial cell proliferation reflects the antiproliferative action of TGF-beta1 on corneal epithelial cells, tested here in single-cell clonal growth assays alongside GDF-5. The abstract reports that GDF-5 inhibited proliferation of corneal epithelial and stromal cells and that TGF-beta1 was used in the same proliferation assays, but it does not state TGF-beta1's specific result, so the antiproliferative effect of TGF-beta1 here rests on the uncached full text. This cytostatic effect is a downstream response to TGF-beta1 receptor binding and SMAD signaling, peripheral to the core activity, so it is kept as non-core. |
| GO:0050680 negative regulation of epithelial cell proliferation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of epithelial cell proliferation. Reason: negative regulation of epithelial cell proliferation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 modulates this cellular behaviour via receptor binding and SMAD-dependent gene regulation in target cells; a real but context-dependent downstream effect of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0050680 negative regulation of epithelial cell proliferation | IMP PMID:16943770 Targeted inhibition of p57 and p15 blocks transforming growt... | KEEP AS NON CORE | Summary: negative regulation of epithelial cell proliferation. Reason: GO:0050680 negative regulation of epithelial cell proliferation. TGF-beta1 (and TGF-beta2) inhibit proliferation of primary human limbal epithelial cells, acting through upregulation of the cyclin-dependent kinase inhibitors p57 and p15 that are required for the growth-inhibitory response. Cytostasis is a classic but cell-type-specific downstream consequence of TGF-beta1/SMAD signaling (CDKI induction and G1 arrest), not a core molecular activity of the secreted ligand; non-core. Supporting Evidence: PMID:16943770 TGF-Ξ²1 or TGF-Ξ²2 significantly inhibited primary cultured human limbal epithelial cell proliferation measured by BrdU incorporation and MTT assay |
| GO:0050714 positive regulation of protein secretion | IDA PMID:18505915 Transforming growth factor-beta1, transforming growth factor... | KEEP AS NON CORE | Summary: positive regulation of protein secretion. Reason: GO:0050714 positive regulation of protein secretion is supported by TGF-beta-1 (with -beta2/-beta3) inducing pro-MMP secretion (and active MMP secretion/invasion on collagen matrix) in ovarian cancer cells. Stimulation of MMP secretion is a downstream transcriptional/secretory output of TGFBR signaling and here is Smad3-independent for secretion; either way it is a consequence of the core receptor-binding function and is non-core. Supporting Evidence: PMID:18505915 TGF-beta1, TGF-beta2, and TGF-beta3 induced pro-matrix metalloproteinase (MMP) secretion |
| GO:0050714 positive regulation of protein secretion | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: positive regulation of protein secretion. Reason: positive regulation of protein secretion is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 modulates the secretion of downstream proteins indirectly through receptor binding and SMAD signaling in responding cells, rather than executing the secretory process itself; retained as a genuine but non-core regulatory consequence. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0050729 positive regulation of inflammatory response | IMP PMID:32141990 miR-4286/TGF-Ξ²1/Smad3-Negative Feedback Loop Ameliorated Vas... | KEEP AS NON CORE | Summary: positive regulation of inflammatory response. Reason: GO:0050729 positive regulation of inflammatory response. PMID:32141990 shows directly that knocking down TGF-beta1 abolishes the ox-LDL-induced inflammatory response of human umbilical vascular endothelial cells, so TGF-beta1 positively regulates the inflammatory response in this atherosclerosis context. This is a tissue- and stimulus-specific downstream consequence of receptor engagement and Smad3 signaling, not a core molecular function of the cytokine. Supporting Evidence: PMID:32141990 Silence of TGF-Ξ²1 reversed the inductive effect of ox-LDL on apoptosis and inflammatory response of HUVECs. |
| GO:0050765 negative regulation of phagocytosis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of phagocytosis. Reason: negative regulation of phagocytosis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0050832 defense response to fungus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: defense response to fungus. Reason: defense response to fungus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 influences this process indirectly through receptor binding and SMAD-dependent signaling in target cells; a genuine but downstream, non-core consequence of the pleiotropic secreted cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0050921 positive regulation of chemotaxis | IDA PMID:18555217 Differential involvement of TGF-beta1 in mediating the motog... | KEEP AS NON CORE | Summary: positive regulation of chemotaxis. Reason: GO:0050921 positive regulation of chemotaxis generalizes the directed-migration readout of this study (a transmembrane migration assay in which TGF-beta1 stimulated motility of endothelial, fibroblast and tumour cells). The abstract reports stimulation of cell migration but does not use the word chemotaxis, so no sentence specifically substantiates this exact term; the chemotactic framing rests on the uncached full text. The term is in any case a downstream motility response to TGF-beta1 receptor binding and SMAD signaling, peripheral to the core cytokine-receptor function, so it is retained as non-core. |
| GO:0051130 positive regulation of cellular component organization | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: positive regulation of cellular component organization. Reason: positive regulation of cellular component organization is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0051240 positive regulation of multicellular organismal process | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: positive regulation of multicellular organismal process. Reason: positive regulation of multicellular organismal process is an electronic (IEA) annotation under GO_REF:0000117. TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0051247 positive regulation of protein metabolic process | IDA PMID:15219857 Up-regulation of acyl-coenzyme A:cholesterol acyltransferase... | KEEP AS NON CORE | Summary: positive regulation of protein metabolic process. Reason: GO:0051247 positive regulation of protein metabolic process. PMID:15219857 shows TGF-beta1 increases ACAT-1 protein expression two- to threefold (with a parallel rise in ACAT activity) during macrophage differentiation, a concrete instance of positively regulating a protein's abundance downstream of Smad signaling. This is a very broad downstream metabolic-regulation term, not a core molecular activity of the ligand. Supporting Evidence: PMID:15219857 TGF-beta1 increased ACAT-1 protein expression by two- to threefold when added during differentiation of human monocytes into macrophages. |
| GO:0051280 negative regulation of release of sequestered calcium ion into cytosol | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of release of sequestered calcium ion into cytosol. Reason: negative regulation of release of sequestered calcium ion into cytosol is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this ion-handling effect is a downstream consequence of TGF-beta-1 receptor signaling in responding cells, not a core activity of the secreted ligand. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0051897 positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction | IDA PMID:18625725 Transforming growth factor beta engages TACE and ErbB3 to ac... | KEEP AS NON CORE | Summary: positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction. Reason: GO:0051897 positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transduction. PMID:18625725 shows TGF-beta activates PI3K/Akt in HER2-overexpressing cells, acting through the TACE-ErbB3 ligand-shedding route rather than the canonical Smad pathway. This non-canonical PI3K/Akt branch is a downstream, context-specific consequence of TGF-beta1 receptor engagement, not a core molecular activity. Supporting Evidence: PMID:18625725 transforming growth factor beta (TGF-beta) activated phosphatidylinositol-3 kinase (PI3K)/Akt and enhanced survival and migration. |
| GO:0055010 ventricular cardiac muscle tissue morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: ventricular cardiac muscle tissue morphogenesis. Reason: ventricular cardiac muscle tissue morphogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0055010 ventricular cardiac muscle tissue morphogenesis | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: ventricular cardiac muscle tissue morphogenesis. Reason: ventricular cardiac muscle tissue morphogenesis is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0060312 regulation of blood vessel remodeling | NAS PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: regulation of blood vessel remodeling. Reason: Regulation of blood vessel remodeling (NAS) captures TGF-beta-1's role in abdominal aortic aneurysm: the study frames TGF-beta as protective, limiting aortic wall expansion by driving a profibrotic, collagen-accumulating response. This is a high-level physiological/pathological outcome of TGF-beta signaling in the vessel wall, an indirect consequence of its receptor binding and SMAD activity rather than a core molecular function, so it is kept non-core. Supporting Evidence: PMID:22269326 Our study supports the protective role of TGF-Ξ² in limiting AAA disease and offers a miR-29βbased mechanism. |
| GO:0060312 regulation of blood vessel remodeling | TAS PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: regulation of blood vessel remodeling. Reason: A traceable author-statement (TAS) counterpart to row 358, asserting TGF-beta-1's involvement in blood vessel remodeling in the aneurysm setting, where the paper concludes TGF-beta plays a protective role in limiting aortic remodeling/expansion. As a context-specific vascular process downstream of TGF-beta signaling, not a direct activity of the secreted protein, it remains non-core. Supporting Evidence: PMID:22269326 Our study supports the protective role of TGF-Ξ² in limiting AAA disease and offers a miR-29βbased mechanism. |
| GO:0060325 face morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: face morphogenesis. Reason: face morphogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0060364 frontal suture morphogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: frontal suture morphogenesis. Reason: frontal suture morphogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:17438144 Smad7 antagonizes transforming growth factor beta signaling ... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:17999987 Loss of type III transforming growth factor beta receptor ex... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:18453574 Activation of a TGF-beta-specific multistep gene expression ... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:19366691 Transforming growth factor beta1 signaling via interaction w... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:19736306 Endoglin phosphorylation by ALK2 contributes to the regulati... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:25196641 Inhibition of TGF-Ξ²/SMAD3/NF-ΞΊB signaling by microRNA-491 is... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:25893292 Syntenin regulates TGF-Ξ²1-induced Smad activation and the ep... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:26634652 Valve Endothelial Cell-Derived TgfΞ²1 Signaling Promotes Nucl... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:27693460 Vascular mimicry formation is promoted by paracrine TGF-Ξ² an... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:28467929 PPARΞ³ Links BMP2 and TGFΞ²1 Pathways in Vascular Smooth Muscl... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:29167509 Cartilage intermediate layer protein 1 (CILP1): A novel medi... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:31023188 LRP1 Deficiency in Vascular SMC Leads to Pulmonary Arterial ... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| 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: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IEA GO_REF:0000107 | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IGI PMID:22714950 MicroRNA-181a regulates local immune balance by inhibiting p... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IMP PMID:26908446 MicroRNA-323-3p inhibits cell invasion and metastasis in pan... | ACCEPT | Summary: Positive regulation of SMAD protein signal transduction. Reason: Core: TGF-beta-1 activates SMAD signaling. |
| GO:0070168 negative regulation of biomineral tissue development | IDA PMID:26634652 Valve Endothelial Cell-Derived TgfΞ²1 Signaling Promotes Nucl... | KEEP AS NON CORE | Summary: negative regulation of biomineral tissue development. Reason: GO:0070168 negative regulation of biomineral tissue development reflects TGF-beta-1 restraining osteoblast-like differentiation and calcific matrix deposition in valve interstitial cells; endothelial loss of Tgfb1 leads to calcific aortic valve disease, so the ligand normally suppresses this biomineralization. This anti-calcific effect is a downstream tissue consequence of receptor binding and SMAD-dependent maintenance of Sox9, hence non-core relative to the core receptor-binding activity. Supporting Evidence: PMID:26634652 loss of TgfΞ²1 in the endothelium leads to reduced Sox9 expression and calcific aortic valve disease |
| GO:0070168 negative regulation of biomineral tissue development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: negative regulation of biomineral tissue development. Reason: negative regulation of biomineral tissue development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0070374 positive regulation of ERK1 and ERK2 cascade | IDA PMID:25310401 Sustained induction of collagen synthesis by TGF-Ξ² requires ... | KEEP AS NON CORE | Summary: positive regulation of ERK1 and ERK2 cascade. Reason: Positive regulation of the ERK1/ERK2 cascade reflects TGF-beta-1's non-canonical (SMAD-independent) signaling: it activates ERKs, which in this study drive repression of TM4SF20 and the resulting RIP of CREB3L1. ERK activation is a downstream, non-canonical branch of TGF-beta signaling distinct from the protein's core receptor-binding and SMAD-initiating function, so the annotation is correctly non-core. Supporting Evidence: PMID:25310401 TGF-Ξ² also activates Smad-independent non-canonical pathways, which include activation of extracellular signal-regulated kinases (ERKs) |
| GO:0070723 response to cholesterol | IDA PMID:17878231 Cholesterol suppresses cellular TGF-beta responsiveness: imp... | KEEP AS NON CORE | Summary: response to cholesterol. Reason: GO:0070723 response to cholesterol is supported by the demonstration that cholesterol loading suppresses or attenuates TGF-beta responsiveness across cell types (reduced SMAD2 phosphorylation, PAI-1 induction and growth inhibition), while cholesterol depletion enhances it. The TGF-beta signaling system thus responds to cellular cholesterol levels; this is a regulatory-input/environmental-response property modulating the pathway, downstream and peripheral to the core receptor-binding function, hence non-core. Supporting Evidence: PMID:17878231 cholesterol treatment suppresses or attenuates TGF-beta responsiveness in all cell types studied |
| GO:0071260 cellular response to mechanical stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to mechanical stimulus. Reason: cellular response to mechanical stimulus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of mechanical stimulus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0071333 cellular response to glucose stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to glucose stimulus. Reason: cellular response to glucose stimulus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of glucose stimulus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0071404 cellular response to low-density lipoprotein particle stimulus | IMP PMID:32141990 miR-4286/TGF-Ξ²1/Smad3-Negative Feedback Loop Ameliorated Vas... | KEEP AS NON CORE | Summary: cellular response to low-density lipoprotein particle stimulus. Reason: GO:0071404 cellular response to low-density lipoprotein particle stimulus. In PMID:32141990 TGF-beta1 is induced/activated by oxidized LDL in endothelial cells, i.e. here TGF-beta1 is a responder whose expression and activity change as part of the cellular response to a modified LDL particle. This is an upstream-stimulus/expression relationship specific to the vascular-injury setting, not a core molecular activity of the secreted ligand. Supporting Evidence: PMID:32141990 TGF-Ξ²1 was activated by ox-LDL in human umbilical vascular endothelial cells (HUVECs). |
| GO:0071456 cellular response to hypoxia | IMP PMID:31368162 HIF1A/miR-20a-5p/TGFΞ²1 axis modulates adipose-derived stem c... | KEEP AS NON CORE | Summary: cellular response to hypoxia. Reason: GO:0071456 cellular response to hypoxia reflects TGF-beta-1 being an output of the hypoxic response: in adipose-derived stem cells HIF1A and TGFbeta1 expression rise under hypoxia (via HIF1A repressing miR-20a, which otherwise targets TGFB1). This places TGF-beta-1 as a hypoxia-regulated effector rather than performing a hypoxia-sensing activity itself, so it is a non-core, context-specific role downstream of the hypoxia/HIF1A axis. Supporting Evidence: PMID:31368162 TGFΞ²1 expressions were increased by hypoxia |
| GO:0071479 cellular response to ionizing radiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to ionizing radiation. Reason: cellular response to ionizing radiation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of ionizing radiation; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0071549 cellular response to dexamethasone stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to dexamethasone stimulus. Reason: cellular response to dexamethasone stimulus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of dexamethasone stimulus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0071560 cellular response to transforming growth factor beta stimulus | IDA PMID:19736306 Endoglin phosphorylation by ALK2 contributes to the regulati... | ACCEPT | Summary: Cellular response to transforming growth factor beta stimulus. Reason: Core: cells respond to TGF-beta-1. |
| GO:0071560 cellular response to transforming growth factor beta stimulus | IDA PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | ACCEPT | Summary: Cellular response to transforming growth factor beta stimulus. Reason: Core: cells respond to TGF-beta-1. |
| GO:0071560 cellular response to transforming growth factor beta stimulus | IEA GO_REF:0000117 | ACCEPT | Summary: Cellular response to transforming growth factor beta stimulus. Reason: Core: cells respond to TGF-beta-1. |
| GO:0071560 cellular response to transforming growth factor beta stimulus | IGI PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | ACCEPT | Summary: Cellular response to transforming growth factor beta stimulus. Reason: Core: cells respond to TGF-beta-1. |
| GO:0071677 positive regulation of mononuclear cell migration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: positive regulation of mononuclear cell migration. Reason: positive regulation of mononuclear cell migration is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a master immunomodulatory cytokine, but its effect on this immune process is mediated through receptor-driven SMAD transcriptional output in target cells; a genuine but downstream immunoregulatory role, non-core relative to the ligand's receptor-binding function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0071895 odontoblast differentiation | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: odontoblast differentiation. Reason: odontoblast differentiation is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 directs this differentiation program through receptor-driven SMAD signaling in target cells; a genuine but downstream, context-dependent role of the secreted cytokine rather than a core molecular activity. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0071895 odontoblast differentiation | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: odontoblast differentiation. Reason: odontoblast differentiation is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 directs this differentiation program through receptor-driven SMAD signaling in target cells; a genuine but downstream, context-dependent role of the secreted cytokine rather than a core molecular activity. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:0072562 blood microparticle | HDA PMID:22516433 Proteomic analysis of microvesicles from plasma of healthy d... | KEEP AS NON CORE | Summary: blood microparticle. Reason: Detected by high-throughput proteomics in circulating blood microparticles, consistent with the secreted cytokine being carried in the circulation; a real but non-core transport/storage pool. |
| GO:0085029 extracellular matrix assembly | IDA PMID:19734317 Mesenchymal stem cells produce Wnt isoforms and TGF-beta1 th... | KEEP AS NON CORE | Summary: extracellular matrix assembly. Reason: GO:0085029 extracellular matrix assembly. The paper demonstrates that TGF-Ξ²1 released by mesenchymal stem cells drives extracellular matrix production (procollagen/COL1A1 gene expression) by lung fibroblasts, one of the two hallmarks of fibrogenesis. The evidence directly supports TGFB1-driven ECM/collagen production (which feeds matrix formation) rather than the ECM assembly/cross-linking step per se; this is a downstream consequence of TGFB1/SMAD signaling in target cells and is retained as non-core. Supporting Evidence: PMID:19734317 fibroblast proliferation and extracellular matrix production, are two key features of lung fibrogenesis |
| GO:0085029 extracellular matrix assembly | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: extracellular matrix assembly. Reason: extracellular matrix assembly is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 is a strong driver of matrix deposition, but the biosynthetic/assembly steps are performed by collagen and ECM machinery in responding cells; for the ligand this is a downstream SMAD-dependent transcriptional consequence rather than a core activity. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| 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. Reason: positive regulation of branching involved in ureteric bud morphogenesis is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0090263 positive regulation of canonical Wnt signaling pathway | IDA PMID:12893825 Transforming growth factor-beta-mediated chondrogenesis of h... | KEEP AS NON CORE | Summary: positive regulation of canonical Wnt signaling pathway. Reason: GO:0090263 positive regulation of canonical Wnt signaling pathway reflects TGF-beta-1-mediated MAP kinase activation controlling WNT-7A expression and Wnt/beta-catenin-TCF signaling during chondrogenesis of mesenchymal progenitor cells. This is crosstalk downstream of receptor binding (via non-canonical MAPK branches feeding into Wnt), a context-specific consequence of the core function, hence non-core. Supporting Evidence: PMID:12893825 TGF-beta1-mediated MAP kinase activation also controls WNT-7A gene expression and Wnt-mediated signaling through the intracellular beta-catenin-TCF pathway |
| GO:0090263 positive regulation of canonical Wnt signaling pathway | IDA PMID:15040835 Cooperation between TGF-beta and Wnt pathways during chondro... | KEEP AS NON CORE | Summary: positive regulation of canonical Wnt signaling pathway. Reason: GO:0090263 positive regulation of canonical Wnt signaling pathway captures crosstalk in which TGF-beta1 upregulates multiple Wnt ligands and the co-receptor LRP5 and increases nuclear accumulation and stability of beta-catenin in marrow stromal cells. This is a signaling-crosstalk effect downstream of TGF-beta1/SMAD activation, one mechanism by which TGF-beta1 steers chondrocyte-versus-adipocyte fate, and is peripheral to the core receptor-binding function, so it is non-core. Supporting Evidence: PMID:15040835 increased nuclear accumulation and stability of beta-catenin in KM101 cells |
| GO:0090263 positive regulation of canonical Wnt signaling pathway | IMP PMID:25605017 Reduction of miR-29c enhances pancreatic cancer cell migrati... | KEEP AS NON CORE | Summary: positive regulation of canonical Wnt signaling pathway. Reason: GO:0090263 positive regulation of canonical Wnt signaling pathway. In pancreatic cancer cells TGF-Ξ²/Smad3 represses miR-29c, which de-represses Wnt upstream regulators and thereby activates the canonical Wnt/Ξ²-catenin cascade. TGFB1's positive effect on Wnt signaling is thus indirect crosstalk operating through an induced reduction in a microRNA, a cell-context-specific downstream consequence of TGFB1/SMAD signaling rather than a core molecular activity, so it is non-core. Supporting Evidence: PMID:25605017 transforming growth factor-Ξ² (TGF-Ξ²) inhibited miR-29c expression, leading to Wnt activation |
| GO:0097191 extrinsic apoptotic signaling pathway | IDA PMID:15334054 Hepatitis C viral proteins interact with Smad3 and different... | KEEP AS NON CORE | Summary: extrinsic apoptotic signaling pathway. Reason: Annotates TGF-beta-1 to the extrinsic apoptotic signaling pathway. The abstract reports that HCV core, NS3 and the subgenomic replicon attenuate TGF-beta/Smad3-mediated apoptosis, indicating TGF-beta-1 can promote apoptosis via Smad3, but it does not specify the extrinsic (death-receptor) branch. Apoptosis induction is a downstream cellular consequence of receptor/SMAD signaling, hence non-core. No verbatim sentence substantiates the extrinsic-pathway specificity; that distinction rests on the uncached full text. |
| GO:0097191 extrinsic apoptotic signaling pathway | IDA PMID:26572508 Rotavirus-induced miR-142-5p elicits proviral milieu by targ... | KEEP AS NON CORE | Summary: extrinsic apoptotic signaling pathway. Reason: GO:0097191 extrinsic apoptotic signaling pathway reflects TGF-beta-1 promoting apoptosis via non-canonical signaling in HT29 cells (suppressed by rotavirus-induced miR-142-5p). Pro-apoptotic signaling is a downstream consequence of receptor engagement, hence non-core. The abstract supports a TGFbeta-induced apoptosis role but does not specify the extrinsic (death-receptor) subtype, which rests on the uncited full text. Supporting Evidence: PMID:26572508 TGFΞ² is induced during rotavirus infection, which may promote apoptosis |
| GO:0097421 liver regeneration | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: liver regeneration. Reason: liver regeneration is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0098586 cellular response to virus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to virus. Reason: cellular response to virus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of virus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:0099126 transforming growth factor beta complex | IEA GO_REF:0000117 | ACCEPT | Summary: Transforming growth factor beta complex. Reason: Core: part of the TGF-beta latent/active complex. |
| GO:0099126 transforming growth factor beta complex | TAS PMID:27252363 Regulation of the Bioavailability of TGF-Ξ² and TGF-Ξ²-Related... | ACCEPT | Summary: Transforming growth factor beta complex. Reason: Core: part of the TGF-beta latent/active complex. |
| GO:0141091 transforming growth factor beta receptor superfamily signaling pathway | IEA GO_REF:0000117 | ACCEPT | Summary: TGF-beta receptor superfamily signaling pathway. Reason: Core signaling pathway. |
| GO:1900126 negative regulation of hyaluronan biosynthetic process | IDA PMID:17324121 Growth factor regulation of hyaluronan synthesis and degrada... | KEEP AS NON CORE | Summary: negative regulation of hyaluronan biosynthetic process. Reason: Annotates TGF-beta-1 to negative regulation of hyaluronan biosynthetic process. The abstract states TGF-beta-1 did not increase hyaluronan-synthesizing activity in dermal fibroblasts (and instead raised hyaluronidase activity); it does not explicitly report a decrease in hyaluronan synthase expression/activity substantiating active negative regulation of biosynthesis. Any such effect is a downstream consequence of TGF-beta-1-SMAD signaling and non-core; the specific claim of negative regulation of biosynthesis rests on the uncached full text, so no verbatim quote is asserted. |
| GO:1900182 positive regulation of protein localization to nucleus | IDA PMID:26634652 Valve Endothelial Cell-Derived TgfΞ²1 Signaling Promotes Nucl... | KEEP AS NON CORE | Summary: positive regulation of protein localization to nucleus. Reason: GO:1900182 positive regulation of protein localization to nucleus reflects Tgfb1 signaling driving nuclear localization (preventing nuclear export) of the transcription factor Sox9 in valve interstitial cells. This is a downstream effect on a transcription-factor effector produced by the SMAD pathway, i.e. a consequence of the core receptor-binding function rather than a direct activity of the secreted ligand, so it is non-core. Supporting Evidence: PMID:26634652 TgfΞ²1 Signaling Promotes Nuclear Localization of Sox9 in Interstitial Cells |
| GO:1901203 positive regulation of extracellular matrix assembly | ISS PMID:24279830 MicroRNA-326 regulates profibrotic functions of transforming... | KEEP AS NON CORE | Summary: positive regulation of extracellular matrix assembly. Reason: GO:1901203 positive regulation of extracellular matrix assembly (evidence ISS) captures TGF-beta1's profibrotic driving of ECM deposition, consistent with its well-established role in lung fibrosis studied here via miR-326 regulation of TGF-beta1. The abstract establishes TGF-beta's profibrotic/fibrogenic role but contains no sentence specifically asserting positive regulation of extracellular matrix assembly, so no verbatim support is given and the ECM-assembly framing rests on broader fibrosis biology/the full text. As an ISS-based, downstream matrix-remodeling consequence of TGF-beta1 signaling, it is peripheral to the core receptor-binding activity and kept as non-core. |
| GO:1901203 positive regulation of extracellular matrix assembly | NAS PMID:27098600 Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting T... | KEEP AS NON CORE | Summary: positive regulation of extracellular matrix assembly. Reason: GO:1901203 positive regulation of extracellular matrix assembly. In human cardiac fibroblasts TGF-beta1 drives fibrogenesis, promoting synthesis of collagen I alpha2 and fibronectin (paralleled by autophagic activation), consistent with TGF-beta1's well-established pro-fibrotic induction of ECM components. This pro-fibrotic ECM deposition is a downstream, context-specific (cardiac fibroblast/fibrosis) transcriptional consequence of TGF-beta1 receptor binding and SMAD signaling rather than a core molecular activity of the ligand; non-core. (Evidence code NAS.) Supporting Evidence: PMID:27098600 TGF-Ξ²1 promotes collagen I Ξ±2 and fibronectin synthesis in HCF |
| GO:1901203 positive regulation of extracellular matrix assembly | NAS PMID:28095798 miR-27b inhibits fibroblast activation via targeting TGFΞ² si... | KEEP AS NON CORE | Summary: positive regulation of extracellular matrix assembly. Reason: GO:1901203 positive regulation of extracellular matrix assembly. The paper states that TGFΞ² activates fibroblasts and enhances collagen synthesis and extracellular matrix deposition, and shows TGF-Ξ²1 induces COL1A1/COL3A1/COL4A1 in lung fibroblasts. This promotion of ECM deposition is a downstream SMAD-dependent transcriptional/synthetic output of TGFB1 signaling in the target fibroblast rather than a direct molecular activity of the ligand, so the annotation is kept as a non-core consequence. Supporting Evidence: PMID:28095798 TGFΞ² activates fibroblasts and enhances collagen synthesis and extracellular matrix deposition |
| GO:1901203 positive regulation of extracellular matrix assembly | TAS PMID:22269326 Inhibition of microRNA-29b reduces murine abdominal aortic a... | KEEP AS NON CORE | Summary: positive regulation of extracellular matrix assembly. Reason: Positive regulation of extracellular matrix assembly reflects TGF-beta-1 driving collagen/ECM deposition in the aortic wall; in this study TGF-beta1 increased collagen synthesis, promoting fibrosis and matrix accumulation. Promoting ECM assembly is a downstream profibrotic outcome of TGFBR binding and SMAD-mediated transcription of matrix genes, not a core molecular activity of the ligand, so non-core is appropriate. Supporting Evidence: PMID:22269326 Collagen synthesis was increased in TGF-Ξ²1βtreated cells compared with that in an untreated control group. |
| GO:1902074 response to salt | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: response to salt. Reason: response to salt is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of salt; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:1902462 positive regulation of mesenchymal stem cell proliferation | IGI PMID:22714950 MicroRNA-181a regulates local immune balance by inhibiting p... | KEEP AS NON CORE | Summary: positive regulation of mesenchymal stem cell proliferation. Reason: Annotates TGF-beta-1 to positive regulation of mesenchymal stem cell proliferation (IGI). The paper shows miR-181a blocks TGF-beta signaling (downregulating TGFBR1/TGFBRAP1) and prevents MSC proliferation, implying intact TGF-beta signaling supports MSC proliferation. This genetic-interaction inference links TGF-beta-1 to MSC proliferation only indirectly, via a downstream receptor-signaling output, so it is non-core. The abstract contains no verbatim statement of TGF-beta-1 promoting MSC proliferation, so no quote is asserted. |
| GO:1902893 regulation of miRNA transcription | IMP NOT PMID:18548003 SMAD proteins control DROSHA-mediated microRNA maturation. | ACCEPT | Summary: Curated NOT annotation; TGF-beta-1 does not regulate this miRNA transcription. Reason: This is a curated NOT (negated) annotation reporting that TGF-beta-1 does not regulate this miRNA transcription. Keep it as the machine-readable record of that negative finding rather than describing it as a positive non-core role. |
| GO:1902894 negative regulation of miRNA transcription | IMP PMID:25605017 Reduction of miR-29c enhances pancreatic cancer cell migrati... | KEEP AS NON CORE | Summary: negative regulation of miRNA transcription. Reason: GO:1902894 negative regulation of miRNA transcription. The paper shows the TGF-Ξ²/Smad3 pathway decreases miR-29c by Smad3 binding directly to an element in the MIR29C promoter, repressing its transcription. This transcriptional repression of a microRNA is the downstream nuclear output of the TGFB1/SMAD3 cascade executed by SMAD3 in the responding cell, not a molecular activity of the secreted TGFB1 ligand itself, so it is retained as a non-core consequence. Supporting Evidence: PMID:25605017 the TGF-Ξ²/Smad3 pathway decreases miR-29c expression by directly targeting the MIR29C promoter in PANC cells |
| GO:1902895 positive regulation of miRNA transcription | IDA PMID:26311719 MicroRNA-143 Activation Regulates Smooth Muscle and Endothel... | KEEP AS NON CORE | Summary: positive regulation of miRNA transcription. Reason: Annotates TGF-beta-1 to positive regulation of miRNA transcription (IDA). The paper maps TGF-beta/Smad signaling as one of the pathways regulating transcription of the miR-143/145 pri-miR cluster in pulmonary artery smooth muscle cells. Driving microRNA transcription is a downstream Smad-dependent transcriptional output of TGF-beta-1 receptor signaling, so it is non-core relative to the ligand's receptor-binding function. Supporting Evidence: PMID:26311719 transforming growth factor-Ξ² (Smads), and hypoxia (hypoxia response element), that regulated levels of all pri-miR stem loop transcription |
| GO:1902895 positive regulation of miRNA transcription | IDA PMID:26493107 miRNA-34a reduces neointima formation through inhibiting smo... | KEEP AS NON CORE | Summary: positive regulation of miRNA transcription. Reason: GO:1902895 positive regulation of miRNA transcription is cited to a study of miR-34a, P53 and Notch1 in vascular smooth muscle cell proliferation/migration and neointima formation; the abstract does not mention TGF-beta1 at all, so no sentence substantiates a role for TGFB1 in positively regulating miRNA transcription, and any such link rests on the uncached full text. Per curation policy this experimental (IDA) annotation is not removed on the basis of an abstract-only cache; the term is in any case a downstream transcriptional output of signaling and is retained as non-core pending full-text verification. |
| GO:1903077 negative regulation of protein localization to plasma membrane | IDA PMID:21168935 Tyrosine phosphorylation of VE-cadherin and claudin-5 is ass... | KEEP AS NON CORE | Summary: negative regulation of protein localization to plasma membrane. Reason: Annotates TGF-beta-1 to negative regulation of protein localization to plasma membrane. The paper reports TGF-beta-1 drives tyrosine phosphorylation and dose/time-dependent decreases in the junctional plasma-membrane proteins VE-cadherin and claudin-5, underlying increased endothelial permeability. The abstract frames this as decreased expression/phosphorylation rather than explicitly as loss of plasma-membrane localization, so the specific localization claim rests on the uncached full text and no verbatim quote is asserted. The effect is a downstream consequence of TGF-beta-1 receptor signaling on endothelial junctions, hence non-core. |
| GO:1903077 negative regulation of protein localization to plasma membrane | IDA PMID:24586048 TGF-Ξ²-inducible microRNA-183 silences tumor-associated natur... | KEEP AS NON CORE | Summary: negative regulation of protein localization to plasma membrane. Reason: GO:1903077 negative regulation of protein localization to plasma membrane. The paper shows TGF-Ξ²1 depletes DAP12 (via induced miR-183), causing loss of surface (plasma-membrane) expression of the NK receptors NKp44 and KIR2DS4 while their cytoplasmic protein stores remain intact, i.e. TGF-Ξ²1 selectively blocks their surface membrane translocation. This effect on receptor plasma-membrane localization is several steps downstream of TGFB1 receptor binding/SMAD signaling (through miR-183 and DAP12) and is a non-core, context-specific consequence rather than a direct molecular activity of TGFB1. Supporting Evidence: PMID:24586048 TGF-Ξ² does not disrupt NKp44 or KIR2DS4 protein abundance but alters surface membrane translocation |
| GO:1904018 positive regulation of vasculature development | IDA PMID:27693460 Vascular mimicry formation is promoted by paracrine TGF-Ξ² an... | KEEP AS NON CORE | Summary: positive regulation of vasculature development. Reason: GO:1904018 positive regulation of vasculature development. PMID:27693460 shows paracrine/recombinant TGF-beta1 promotes vascular mimicry (tumor-cell-formed vascular-like channels) in hepatocellular carcinoma by upregulating VE-cadherin, MMP2 and laminin5-gamma2 via TGF-betaR1. This is a tumor-context pro-angiogenic/vasculature-forming effect downstream of receptor/Smad signaling, non-core relative to receptor binding. Supporting Evidence: PMID:27693460 Similar to CM-CAF, recombinant TGF-Ξ²1 and SDF1 induced VM formation. |
| GO:1904894 positive regulation of receptor signaling pathway via STAT | IDA PMID:28467929 PPARΞ³ Links BMP2 and TGFΞ²1 Pathways in Vascular Smooth Muscl... | KEEP AS NON CORE | Summary: positive regulation of receptor signaling pathway via STAT. Reason: Annotates TGF-beta-1 to positive regulation of STAT receptor signaling. The paper shows TGF-beta-1 drives a Stat3-dependent (TGF-beta-1-Stat3-FoxO1) axis in vascular smooth muscle cells, which PPARgamma restrains by binding Stat3. Engagement of a STAT branch is a non-canonical, context-dependent downstream arm of TGF-beta-1 signaling initiated after receptor binding, hence non-core to the primary receptor-binding/SMAD function. Supporting Evidence: PMID:28467929 pro-proliferative TGFΞ²1-Stat3-FoxO1 axis in VSMCs |
| GO:1905005 regulation of epithelial to mesenchymal transition involved in endocardial cushion formation | ISS NOT GO_REF:0000024 | ACCEPT | Summary: Curated NOT annotation; TGF-beta-1 is not involved in this endocardial-cushion EMT regulation. Reason: This is a curated NOT (negated) annotation; keep it as the machine-readable record that TGF-beta-1 does not regulate epithelial-to-mesenchymal transition in endocardial cushion formation, rather than describing it as a positive non-core role. |
| GO:1905641 cellular response to acetaldehyde | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to acetaldehyde. Reason: cellular response to acetaldehyde is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of acetaldehyde; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:1990314 cellular response to insulin-like growth factor stimulus | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: cellular response to insulin-like growth factor stimulus. Reason: cellular response to insulin-like growth factor stimulus is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). this term records that TGF-beta-1 expression or activity is modulated in the context of insulin-like growth factor stimulus; it is a context-specific regulatory relationship of the secreted cytokine, not a core molecular function. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:1990402 embryonic liver development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: embryonic liver development. Reason: embryonic liver development is an electronic transfer from an experimentally-annotated ortholog via Ensembl Compara (IEA, GO_REF:0000107). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this electronic annotation, so no supporting quote is asserted. |
| GO:1990402 embryonic liver development | ISS GO_REF:0000024 | KEEP AS NON CORE | Summary: embryonic liver development. Reason: embryonic liver development is a sequence-similarity transfer from an experimentally-characterized ortholog (ISS, GO_REF:0000024). TGF-beta-1 signaling helps pattern this developmental/morphogenetic program, but the ligand's own role is to bind its receptors and drive SMAD-dependent transcription; the developmental outcome is a downstream, tissue-context-dependent consequence rather than a core activity of the cytokine. No primary publication is attached to this annotation, so no supporting quote is asserted. |
| GO:2000048 negative regulation of cell-cell adhesion mediated by cadherin | IDA PMID:18593713 Smad7 stabilizes beta-catenin binding to E-cadherin complex ... | KEEP AS NON CORE | Summary: negative regulation of cell-cell adhesion mediated by cadherin. Reason: GO:2000048 negative regulation of cell-cell adhesion mediated by cadherin captures the loosening of adherens junctions during TGF-beta1 signaling. This study is actually about Smad7 (an inhibitory SMAD that antagonizes TGF-beta signaling) promoting cell-cell adhesion by stabilizing the beta-catenin/E-cadherin complex, so the negative-regulation annotation on TGFB1 is the inferred inverse: active TGF-beta/SMAD signaling reduces cadherin-mediated adhesion. The abstract describes Smad7's pro-adhesive effect, not a direct statement that TGF-beta1 negatively regulates cadherin adhesion, so that attribution rests on the uncached full text. The term is a downstream, indirect consequence of signaling (EMT-associated junction disassembly), peripheral to the core cytokine-receptor activity, and is retained as non-core. |
| GO:2000343 positive regulation of chemokine (C-X-C motif) ligand 2 production | IMP PMID:32141990 miR-4286/TGF-Ξ²1/Smad3-Negative Feedback Loop Ameliorated Vas... | KEEP AS NON CORE | Summary: positive regulation of chemokine (C-X-C motif) ligand 2 production. Reason: GO:2000343 positive regulation of chemokine (C-X-C motif) ligand 2 production. This is one more component of the ox-LDL-induced endothelial inflammatory program that TGF-beta1 drives in PMID:32141990. CXCL2 induction is a downstream, context-specific output of receptor binding plus Smad3 signaling rather than a core activity. The cached abstract reports only a general inflammatory response and does not name CXCL2, so the CXCL2-specific claim rests on the curator's full-text reading (not cached). |
| GO:2000353 positive regulation of endothelial cell apoptotic process | IMP PMID:32141990 miR-4286/TGF-Ξ²1/Smad3-Negative Feedback Loop Ameliorated Vas... | KEEP AS NON CORE | Summary: positive regulation of endothelial cell apoptotic process. Reason: GO:2000353 positive regulation of endothelial cell apoptotic process. PMID:32141990 shows that silencing TGF-beta1 reverses the ox-LDL-induced apoptosis of HUVECs (endothelial cells), so TGF-beta1 promotes endothelial apoptosis in this oxidative-stress context. TGF-beta1 is anti-apoptotic/cytoprotective in many other settings, underscoring that this pro-apoptotic effect is a context-specific downstream consequence of Smad3 signaling, not a core function. Supporting Evidence: PMID:32141990 Silence of TGF-Ξ²1 reversed the inductive effect of ox-LDL on apoptosis and inflammatory response of HUVECs. |
| GO:2000636 positive regulation of primary miRNA processing | IDA PMID:18548003 SMAD proteins control DROSHA-mediated microRNA maturation. | KEEP AS NON CORE | Summary: positive regulation of primary miRNA processing. Reason: GO:2000636 positive regulation of primary miRNA processing. This study shows TGF-beta (and BMP) signaling promotes post-transcriptional maturation of miR-21: receptor-activated R-SMADs are recruited to pri-miR-21 together with the helicase p68, a DROSHA microprocessor subunit, enhancing cropping of pri-miR-21 into pre-miR-21 in a SMAD4-independent manner. Enhancing microprocessor-mediated miRNA processing is a specialized non-canonical downstream branch of TGF-beta1/SMAD signaling (in vascular smooth muscle and cancer cells), not the secreted ligand's core receptor-binding activity; non-core. Supporting Evidence: PMID:18548003 TGF-Ξ² and BMP signalling promotes a rapid increase in expression of mature miR-21 through a post-transcriptional step, promoting the processing of primary transcripts of miR-21 (pri-miR-21) into precursor miR-21 (pre-miR-21) by the DROSHA (also known as RNASEN) complex |
| GO:2000727 positive regulation of cardiac muscle cell differentiation | IDA PMID:25163461 Inhibitory effect of hsa-miR-590-5p on cardiosphere-derived ... | KEEP AS NON CORE | Summary: positive regulation of cardiac muscle cell differentiation. Reason: GO:2000727 positive regulation of cardiac muscle cell differentiation records TGF-beta1 inducing differentiation of cardiosphere-derived (cardiac progenitor) cells, confirmed by qPCR, immunocytochemistry and flow cytometry. This is a tissue-specific developmental outcome downstream of TGF-beta1/SMAD signaling, not the core receptor-binding activity, and is appropriately non-core. Supporting Evidence: PMID:25163461 The differentiation induction of CDCs by TGFB1 was confirmed by |
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Experiment: Cell-type-resolved profiling of SMAD target genes after acute, latency-bypassing TGF-beta-1 stimulation to separate direct transcriptional responses from secondary effects.
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