GDF2 encodes BMP9, a secreted TGF-beta-family cytokine produced as a precursor and processed into a mature dimeric ligand. BMP9 engages ALK1-containing receptor complexes and the co-receptor endoglin to activate SMAD signaling. Its vascular effects depend on endothelial context, and it also influences epithelial differentiation and barrier function. The cleaved prodomain can remain associated with receptor-active mature BMP9.
Curated functional classes representing distinct biological activities. These may be splice variants, cleavage products, or other forms with different functions.
GDF2_MATURE_BMP9PRO_0000033903 (residues 320-429) | GO Term | Evidence | Action | Reason |
|---|---|---|---|
| GO:0001503 ossification | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: BMP9 has experimentally supported osteogenic potential. Reason: Human BMP9 expression induces osteogenic markers and mineralized nodules in the authentic primary abstract. Retain this contextual activity without asserting normal human skeletal necessity. |
| GO:0001503 ossification | TAS PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Retain the contextual bone-formation role. Reason: The original TAS paper discusses earlier skeletal work; independent human-BMP9 mineralization evidence supports the role. Cartilage-marker induction alone is not treated as ossification. |
| GO:0001525 angiogenesis | IMP PMID:23972370 BMP9 mutations cause a vascular-anomaly syndrome with phenot... | KEEP AS NON CORE | Summary: BMP9 contributes to vascular remodeling. Reason: Zebrafish bmp9 perturbation supports the developmental role; human variant assays separately establish ligand defects. No human-ligand fish rescue is inferred. Supporting Evidence: |
| GO:0001569 branching involved in blood vessel morphogenesis | IDA PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Vascular branching response. Reason: BMP9 increased PECAM1-positive allantoic vascular area, with disorganized and disconnected vessels (PMID:20406889, Figure 2). Retain this contextual morphogenetic response. Supporting Evidence: |
| GO:0001569 branching involved in blood vessel morphogenesis | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: Contextual vascular branching. Reason: Retain the donor-supported morphological response. |
| GO:0001570 vasculogenesis | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Contextual vasculogenesis. Reason: Allantoic vascularization supports the transfer; no human developmental assay is implied. |
| GO:0001937 negative regulation of endothelial cell proliferation | IDA PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Contextual proliferation inhibition. Reason: Human inhibition was reported without displayed data; independent evidence corroborates it. |
| GO:0001938 positive regulation of endothelial cell proliferation | IBA GO_REF:0000033 | KEEP AS NON CORE | Summary: Retain ancestral positive endothelial proliferation. Reason: Actual AN340/PTN008330932 placement and both descendant sources support inheritance. Positive effects are contextual; human self-evidence is legitimate. |
| GO:0001938 positive regulation of endothelial cell proliferation | IDA PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Contextual proliferation promotion. Reason: Cell-count evidence supports the positive effect without a universal direction. Supporting Evidence: |
| GO:0001938 positive regulation of endothelial cell proliferation | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: Contextual proliferation promotion. Reason: Retain the donor-supported electronic conclusion. |
| GO:0005125 cytokine activity | IBA GO_REF:0000033 | ACCEPT | Summary: BMP9 is a conserved extracellular cytokine. Reason: The sequence-verified human target descends from the actual AN0/PTN000218063 cytokine IBD. Its own experimental evidence legitimately seeds that ancestral placement. Human receptor-dependent signaling independently supports this core activity. |
| GO:0005125 cytokine activity | IGI PMID:32082362 MiR-199b-5p Suppresses Tumor Angiogenesis Mediated by Vascul... | ACCEPT | Summary: Human BMP9 supplies a receptor-active cytokine input. Reason: Recombinant human BMP9 induces SMAD signaling in HUVECs; the miR-199b-5p/ALK1 intervention alters that response. The paper therefore assays BMP9 directly despite its microRNA emphasis. This does not make GDF2 the microRNA target. Supporting Evidence: |
| GO:0005515 protein binding | IPI PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | MODIFY | Summary: Receptor-specific binding. Reason: BMP9-dependent reporter responses are blocked by soluble ALK1 (PMID:17068149, Figure 2). BMP receptor binding identifies the functional partner class missing from generic protein binding; cytokine activity captures the ligand role in the core. Proposed replacements: BMP receptor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI Q9UK05-PRO_0000033903 PMID:28564608 Structural Basis of the Human Endoglin-BMP9 Interaction: Ins... | MODIFY | Summary: Mature BMP9 binds its BMP co-receptor endoglin. Reason: Human BMP9 binds endoglin, a BMP receptor-complex co-receptor (PMID:28564608, binding/interface experiments). GO:0070700 identifies this informative receptor-system interaction without assigning endoglin kinase activity. Proposed replacements: BMP receptor binding Supporting Evidence: |
| GO:0005515 protein binding | IPI Q9UK05-PRO_0000033903 PMID:28564608 Structural Basis of the Human Endoglin-BMP9 Interaction: Ins... | MODIFY | Summary: Mature BMP9 binds the BMP type-I receptor ALK1. Reason: The human ALK1–BMP9–ENG pull-down supports the named receptor interaction independently of the modeled ternary geometry. Use BMP receptor binding and preserve the mature-chain target rather than inventing a splice isoform. Proposed replacements: BMP receptor binding Supporting Evidence: |
| GO:0005576 extracellular region | EXP PMID:21710321 BMP9 is produced by hepatocytes and circulates mainly in an ... | ACCEPT | Summary: BMP9 is present extracellularly in circulating forms. Reason: The authentic abstract reports plasma BMP9 and distinguishes precursor from mature prodomain-associated ligand. That supports the location without relying on exact form percentages; the linked erratum’s contents remain unresolved. |
| GO:0005576 extracellular region | EXP PMID:25237187 Regulation of bone morphogenetic protein 9 (BMP9) by redox-d... | ACCEPT | Summary: BMP9 is an extracellular ligand whose stability is regulated. Reason: The authentic abstract describes serum-dependent processing and receptor-active BMP9 forms, consistent with the established secreted location. Disulfide-linked and noncovalent dimers are biochemical states, not alternative splice products. |
| GO:0005576 extracellular region | IBA GO_REF:0000033 | ACCEPT | Summary: The active ligand acts extracellularly. Reason: The actual AN0/PTN000218063 extracellular-region IBD is on the sequence-verified human lineage and agrees with the secreted receptor ligand. Human self-evidence is legitimate; precursor biosynthesis in the secretory pathway does not contradict extracellular mature-ligand activity. |
| GO:0005576 extracellular region | IDA PMID:18309101 Bone morphogenetic protein-9 is a circulating vascular quies... | ACCEPT | Summary: Biologically active BMP9 circulates extracellularly. Reason: Human serum/plasma measurements and BMP9-neutralization of serum-induced SMAD signaling support the existing active extracellular location. The paper’s mouse and chicken angiogenesis tests remain distinct from this human localization evidence. Supporting Evidence: |
| GO:0005576 extracellular region | IEA GO_REF:0000120 | ACCEPT | Summary: The electronic extracellular localization is appropriate. Reason: The incoming InterPro and UniProt subcellular sources agree with the secreted BMP9 ligand and its extracellular receptor engagement. Preserve this location without assigning an additional splice product or assuming that every precursor segment remains in circulating ligand complexes. Supporting Evidence: GO_REF:0000120 file:human/GDF2/GDF2-uniprot.txt |
| GO:0005576 extracellular region | TAS Reactome:R-HSA-8858369 | ACCEPT | Summary: The Reactome participant is extracellular human GDF2. Reason: The actual event input set contains the GDF2 dimer, whose component is the Q9UK05-linked extracellular protein with mature-chain coordinates 320–429. This is target-specific participant support, not localization inferred from the receptor’s plasma-membrane compartment. |
| GO:0006879 intracellular iron ion homeostasis | IEA GO_REF:0000117 | UNDECIDED | Summary: An iron-regulatory relationship is supported, but this cellular assignment remains uncertain. Reason: Hepcidin induction and combined mouse Gdf2/Bmp10 loss support iron regulation, but do not settle this GDF2-specific intracellular claim. GO:0060586 instead concerns extracellular body-fluid iron; it is not an established replacement here. |
| GO:0006879 intracellular iron ion homeostasis | TAS PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | UNDECIDED | Summary: The TAS citation points to earlier hepcidin work, not an iron assay performed in this paper. Reason: The cited paper refers to earlier hepcidin work. Positive later physiology comes from combined Gdf2/Bmp10 loss; isolated GDF2 control of intracellular iron remains unresolved. Reading these sources does not resolve that attribution. |
| GO:0008083 growth factor activity | IDA PMID:19903896 ALK1 signaling regulates early postnatal lymphatic vessel de... | KEEP AS NON CORE | Summary: BMP9 has context-dependent growth-factor activity. Reason: This paper demonstrates human BMP9-dependent SMAD responses, not increased human lymphatic endothelial proliferation. The growth-promoting activity is independently supported by PMID:7664647; retain it without transferring that mitogenic result to this paper’s lymphatic assays. |
| GO:0008083 growth factor activity | IDA PMID:7664647 Bone morphogenetic protein-9 binds to liver cells and stimul... | KEEP AS NON CORE | Summary: Human BMP9 stimulates liver-cell proliferation. Reason: The authentic abstract reports human HepG2 thymidine incorporation and cell counting after recombinant human BMP9, separately from primary rat hepatocytes. This directly supports a contextual mitogenic function and the retained receptor-activation extension; it is not a universal vascular response. Supporting Evidence: |
| GO:0008083 growth factor activity | IEA GO_REF:0000002 | KEEP AS NON CORE | Summary: BMP9 can act as a mitogen in selected cellular contexts. Reason: The family mapping agrees with direct human HepG2 proliferation evidence. Retain growth-factor activity as a contextual facet of the receptor ligand; it does not imply stimulation of every endothelial population. |
| GO:0008156 negative regulation of DNA replication | TAS PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Contextual DNA-synthesis inhibition. Reason: BMP9 reduced bulk HPAEC thymidine incorporation through ALK1/BMPR-II (PMID:19366699). Retain population-level DNA-synthesis regulation; cell-number normalization was not reported, and per-cell replication, cell-cycle redistribution and fork mechanisms were not resolved. GO:0008156 does not require a specific replication-machinery mechanism. |
| GO:0010596 negative regulation of endothelial cell migration | IDA PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | KEEP AS NON CORE | Summary: Contextual migration inhibition. Reason: BMP9 reduced HMVEC-d scratch closure, reversed by soluble ALK1 (PMID:17068149, Figure 5A). Retain contextual migration inhibition. Supporting Evidence: |
| GO:0010628 positive regulation of gene expression | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Downstream gene-expression regulation. Reason: BMP9 induces transcript abundance in HPAECs (PMID:19366699, Figure 3B). Current GO:0045944 ancestry reaches GO:0045893, but not GO:0010628, so the claimed strict-child redundancy is not established. |
| GO:0016525 negative regulation of angiogenesis | TAS PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: BMP9 can inhibit angiogenesis. Reason: BMP9 inhibited sprouting in the mouse sponge assay and circulation in the chick chorioallantoic membrane assay (PMID:18309101, abstract). These contextual antiangiogenic endpoints support the TAS claim without a universal vascular direction. |
| GO:0030308 negative regulation of cell growth | IDA PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | MODIFY | Summary: Proliferation, not size-defined growth. Reason: WST-1 indirectly measures viable-cell number, not the cell-size increase meant by GO cell growth. The stated endothelial proliferation experiment supports GO:0001937; division versus viability remains unresolved. This size/readout mismatch differs from directly assaying population DNA synthesis. Proposed replacements: negative regulation of endothelial cell proliferation Supporting Evidence: |
| GO:0030509 BMP signaling pathway | IBA GO_REF:0000033 | ACCEPT | Summary: BMP signaling is an inherited core ligand function. Reason: The actual AN340/PTN008330932 BMP-signaling assertion lies on the human target lineage. Its single human experimental donor is legitimate ancestral evidence, not circular propagation. The receptor-active ligand executes pathway initiation. |
| GO:0030509 BMP signaling pathway | IDA PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | ACCEPT | Summary: Core ligand signaling. Reason: BMP9 induced HMVEC-d phospho-SMAD1/5/8 and ALK1-dependent reporter responses (PMID:17068149, Figure 1). The ligand initiates signaling. Supporting Evidence: |
| GO:0030509 BMP signaling pathway | IDA PMID:19366699 Bone morphogenetic protein (BMP) and activin type II recepto... | ACCEPT | Summary: Core BMP signaling. Reason: ALK1 knockdown attenuated BMP9-induced SMAD phosphorylation and transcription in HPAECs (PMID:19366699, Figure 3). This supports ligand-driven BMP signaling. Supporting Evidence: |
| GO:0030509 BMP signaling pathway | IDA PMID:19903896 ALK1 signaling regulates early postnatal lymphatic vessel de... | ACCEPT | Summary: BMP9 initiates BMP signaling in human endothelial cells. Reason: Recombinant human BMP9 induces the SMAD6 reporter response and is blocked by ALK1-Fc. Preserve the literal ligand-input context; mouse ALK1-trap phenotypes are separate and do not identify BMP9 as their only ligand. Supporting Evidence: |
| GO:0030509 BMP signaling pathway | IDA PMID:32082362 MiR-199b-5p Suppresses Tumor Angiogenesis Mediated by Vascul... | ACCEPT | Summary: BMP9 is the measured BMP-pathway stimulus. Reason: The original human endothelial experiment measures BMP9-induced phospho-SMAD1/5/8 and ID1. Preserve the literal has_input target context without mistaking the separate microRNA intervention for GDF2 binding or an in-vivo ligand perturbation. Supporting Evidence: |
| GO:0030509 BMP signaling pathway | IDA PMID:32561494 Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Ep... | ACCEPT | Summary: Core epithelial BMP signaling. Reason: BMP9 effects on colonocyte markers were reversed by ALK1-Fc (PMID:32561494, Results). This supports receptor-pathway initiation; the study did not newly measure phospho-SMAD. Preserve the original OR alternatives. Supporting Evidence: |
| GO:0030513 positive regulation of BMP signaling pathway | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Contextual BMP-pathway amplification. Reason: The mouse study reports induction of ALK1 and endoglin and interprets ALK1 expression as positive feedback (PMID:20406889, Discussion). Retain this bounded amplification claim. |
| GO:0030858 positive regulation of epithelial cell differentiation | IDA PMID:32561494 Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Ep... | KEEP AS NON CORE | Summary: Colonocyte differentiation. Reason: BMP9 increased CA1 protein and colonocyte transcripts in primary human colon monolayers; ALK1-Fc reversed the response (PMID:32561494, Results). Retain the contextual differentiation claim. Supporting Evidence: |
| GO:0030858 positive regulation of epithelial cell differentiation | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Contextual epithelial differentiation. Reason: Direct colonocyte evidence supports the electronic assertion. |
| GO:0032757 positive regulation of interleukin-8 production | IDA PMID:19366699 Bone morphogenetic protein (BMP) and activin type II recepto... | KEEP AS NON CORE | Summary: Contextual IL-8 regulation. Reason: Expression supports this context; positive secreted-protein results were not independently recovered. Supporting Evidence: |
| GO:0032924 activin receptor signaling pathway | IDA PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | KEEP AS NON CORE | Summary: Activin-receptor-dependent signaling. Reason: GO:0032924 describes extracellular-ligand signaling through an activin receptor, without requiring an activin-family ligand. Combined ActRIIA/BMPR-II knockdown reduced BMP9 reporter signaling (PMID:17068149, Figure 3), supporting this receptor-defined pathway. Supporting Evidence: |
| GO:0043537 negative regulation of blood vessel endothelial cell migration | TAS PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Contextual endothelial migration inhibition. Reason: The TAS source cites earlier inhibition studies. Human HMVEC-d scratch closure was inhibited in PMID:17068149, Figure 5A; retain that contextual response. |
| GO:0045603 positive regulation of endothelial cell differentiation | IEA GO_REF:0000107 | MARK AS OVER ANNOTATED | Summary: Increased endothelial-cell yield does not isolate increased differentiation. Reason: The 2010 donor study confounds differentiation with increased cell yield. The 2024 Gdf2/Bmp10 double-knockout study additionally supports maintenance of specialized sinusoidal endothelial identity; it does not isolate GDF2-driven acquisition or rate of endothelial differentiation. This narrower overextension judgment preserves both proliferation and identity-maintenance evidence. |
| GO:0045747 positive regulation of Notch signaling pathway | IDA PMID:32561494 Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Ep... | KEEP AS NON CORE | Summary: Upstream Notch regulation. Reason: BMP9 increased HES1, HES5 and JAG1 transcripts in primary human colon monolayers (PMID:32561494, Results). Preserve acts_upstream_of; these responses do not establish direct Notch-receptor binding. Supporting Evidence: |
| GO:0045766 positive regulation of angiogenesis | IDA PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: Contextual angiogenesis promotion. Reason: Mouse allantoic vascular expansion and human-BMP9-transgene xenograft vascularization support contextual angiogenesis promotion (PMID:20406889). Increased area can include disorganized vessels; no universal direction is inferred. Supporting Evidence: |
| GO:0045766 positive regulation of angiogenesis | IEA GO_REF:0000120 | KEEP AS NON CORE | Summary: Contextual angiogenesis promotion. Reason: Retain donor-supported vascular effects without a universal direction. |
| GO:0045893 positive regulation of DNA-templated transcription | IDA PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | TOO GENERAL | Summary: A retained specific child is sufficient. Reason: GO:0045944 is an actual is_a child already present; neither term assigns DNA binding. Supporting Evidence: |
| GO:0045893 positive regulation of DNA-templated transcription | IEA GO_REF:0000107 | TOO GENERAL | Summary: A retained specific transcriptional child captures this response. Reason: Actual GO:0045944 is_a ancestry reaches GO:0045893. Retain the specific polymerase-II response without treating the mouse transfer as false or GDF2 as a DNA-binding protein. |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IDA PMID:19366699 Bone morphogenetic protein (BMP) and activin type II recepto... | KEEP AS NON CORE | Summary: Downstream transcriptional induction. Reason: BMP9 induced ID1/ID2, IL8 and SELE transcripts in HPAECs (PMID:19366699, selected original Results). Preserve the seven alternative inputs as OR. Supporting Evidence: |
| GO:0045944 positive regulation of transcription by RNA polymerase II | IEA GO_REF:0000117 | KEEP AS NON CORE | Summary: Signaling-dependent transcription. Reason: BMP9-induced HPAEC transcript responses support this electronic regulatory assertion (PMID:19366699); they do not assign DNA binding to the ligand. |
| GO:0048514 blood vessel morphogenesis | IDA PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | TOO GENERAL | Summary: Retained vascular children capture this broad morphogenesis term. Reason: Verified part_of children GO:0001569, GO:0001570 and GO:0001525 already provide more specific retained coverage. Supporting Evidence: |
| GO:0051216 cartilage development | TAS PMID:20406889 BMP-9 induces proliferation of multiple types of endothelial... | KEEP AS NON CORE | Summary: BMP9 promotes contextual chondrogenesis. Reason: The cited human mesenchymal-cell study supports cartilage differentiation, corroborated by direct BMP9 micromass experiments. This developmental response is not the defining ligand function. |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:17068149 Identification of BMP9 and BMP10 as functional activators of... | ACCEPT | Summary: Core SMAD activation. Reason: BMP9 increased HMVEC-d phospho-SMAD1/5/8 (PMID:17068149, Figure 1A). The ligand activates receptor-mediated signaling, not kinase catalysis. Supporting Evidence: |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:19366699 Bone morphogenetic protein (BMP) and activin type II recepto... | ACCEPT | Summary: Core SMAD activation. Reason: BMP9 stimulated HPAEC SMAD1/5 and SMAD2 phosphorylation (PMID:19366699, Figure 2). Preserve the three alternative extension groups without assigning ligand kinase activity. Supporting Evidence: |
| GO:0060391 positive regulation of SMAD protein signal transduction | IDA PMID:19903896 ALK1 signaling regulates early postnatal lymphatic vessel de... | ACCEPT | Summary: BMP9 activates a SMAD signaling response. Reason: Human endothelial SMAD6 induction supports this core ligand response. The paper describes correlated phospho-SMAD1/ID1 observations as data not shown, so these are not treated as independently inspected blots. Preserve both extension atoms. Supporting Evidence: |
| GO:0061036 positive regulation of cartilage development | IEA GO_REF:0000107 | KEEP AS NON CORE | Summary: Retain the directly grounded mouse cartilage-regulation transfer. Reason: The actual donor source assays mouse Bmp9 constructs and recombinant human BMP9 in distinct chicken micromass experiments. Both support chondrogenic potential without equating construct and recipient species. |
| GO:0070062 extracellular exosome | HDA PMID:19056867 Large-scale proteomics and phosphoproteomics of urinary exos... | UNDECIDED | Summary: The urinary-exosome target identification remains unverified here. Reason: The original study profiles a low-density urinary fraction chiefly containing exosomes. Its target-level supplemental accession/peptide record was not recovered; preserve the HDA annotation and urinary extension without inferring absence or vesicle-specific residence. Supporting Evidence: |
| GO:0071773 cellular response to BMP stimulus | IDA PMID:19366699 Bone morphogenetic protein (BMP) and activin type II recepto... | TOO GENERAL | Summary: The retained BMP pathway supplies more specific response coverage. Reason: GO:0030509 is actually part_of GO:0071773. The broader response is valid but redundant with the measured pathway. Supporting Evidence: |
| GO:0090100 positive regulation of transmembrane receptor protein serine/threonine kinase signaling pathway | IEA GO_REF:0000117 | TOO GENERAL | Summary: The retained SMAD-signaling child is more specific. Reason: GO:0060391 is an actual is_a child of this broader receptor-pathway regulation term. The supported ligand-dependent response is retained there. |
| GO:1903348 positive regulation of bicellular tight junction assembly | IDA PMID:32561494 Decreased Colonic Activin Receptor-Like Kinase 1 Disrupts Ep... | UNDECIDED | Summary: Barrier response; assembly unresolved. Reason: BMP9 increased junctional transcripts and TEER in primary colon monolayers, but these readouts do not distinguish assembly from maintenance or function. The available readouts leave the assembly-specific interpretation unresolved. Supporting Evidence: |
Loading supporting content…
Download this section (compressed HTML)Q: Which receptor, endothelial state and ligand-presentation features determine whether BMP9 increases or decreases endothelial proliferation?
Q: How do endogenous precursor cleavage, prodomain association and disulfide state determine circulating BMP9 signaling?
Q: What is the contribution of GDF2 alone to hepatic iron regulation and endothelial identity, separately from BMP10 and downstream BMP2/6?
Q: Does the urinary proteomic evidence identify GDF2-derived peptides specifically in extracellular vesicles rather than co-isolated soluble material?
Experiment: Compare matched human endothelial states with quantified receptor levels and purified ligand forms, measuring direct division, survival and migration separately.
Hypothesis: Receptor composition and endothelial differentiation state determine the direction of the BMP9 proliferative response.
Experiment: Compare selective and combined perturbations with cell-resolved iron, hepcidin and endothelial-identity measurements, using ligand-specific rescue.
Hypothesis: GDF2 regulates liver iron balance through endothelial signals that are partly redundant with BMP10.
Loading supporting content…
Download this section (compressed HTML)Loading supporting content…
Download this section (compressed HTML)Loading supporting content…
Download this section (compressed HTML)