Affinage

TGFBR3

Transforming growth factor beta receptor type 3 · UniProt Q03167

Length
851 aa
Mass
93.5 kDa
Annotated
2026-04-28
100 papers in source corpus 42 papers cited in narrative 42 extracted findings

Mechanistic narrative

Synthesis pass · prose summary of the discoveries below

TGFBR3 (betaglycan) is a membrane-anchored proteoglycan co-receptor that orchestrates TGF-β superfamily signaling by presenting ligands to signaling receptors, sequestering ligands in soluble form, and independently modulating Wnt and NF-κB pathways. Its ectodomain contains two TGF-β-binding lobes — an N-terminal endoglin-related domain that mediates TGF-β presentation to TGFBR2 via a hand-off mechanism requiring betaglycan displacement by TGFBR1, and a C-terminal zona pellucida domain that serves as the obligate inhibin A co-receptor, forming ternary complexes with activin type II receptors to antagonize activin signaling in gonadotropes and other tissues (PMID:8391934, PMID:10746731, PMID:27951653, PMID:40011426, PMID:30364975). The shed soluble ectodomain acts as a potent TGF-β antagonist with preferential neutralization of TGF-β2, while its glycosaminoglycan chains independently bind bFGF, differentially regulate Wnt3a signaling (heparan sulfate inhibitory, chondroitin sulfate stimulatory), and modulate TGFBR1–TGFBR2 complex formation (PMID:8106553, PMID:11668175, PMID:27784788, PMID:1556106). Betaglycan also signals in a TGF-β-independent manner through its cytoplasmic domain via p38 MAPK and through β-arrestin 2–mediated NF-κB inhibition, and is required for normal fetal testis development and dose-sensitive kidney morphogenesis (PMID:16413747, PMID:29130787, PMID:19696014, PMID:21533152).

Mechanistic history

Synthesis pass · year-by-year structured walk · 19 steps
  1. 1989 High

    Before the molecular identity of the type III TGF-β receptor was known, this study established that betaglycan exists as both membrane-bound and soluble proteoglycan forms that bind TGF-β via core protein carrying heparan sulfate and chondroitin sulfate GAG chains.

    Evidence Affinity labeling, liposome association, and biochemical fractionation of cell-derived betaglycan

    PMID:2592419

    Open questions at the time
    • Molecular cloning not yet achieved
    • Functional role of GAG chains unknown
    • Mechanism of soluble form generation undefined
  2. 1991 High

    cDNA cloning revealed betaglycan as a transmembrane proteoglycan with an ectodomain carrying GAG chains and a cytoplasmic domain homologous to endoglin, establishing that GAG chains are dispensable for TGF-β binding to the core protein.

    Evidence cDNA cloning, structural domain analysis, biochemical characterization

    PMID:1657406

    Open questions at the time
    • Function of cytoplasmic domain unknown
    • Mechanism of TGF-β presentation not yet demonstrated
  3. 1992 High

    Discovery that betaglycan binds bFGF through its heparan sulfate chains at a site distinct from the TGF-β-binding core protein established betaglycan as a dual-ligand co-receptor with ligand-regulated GAG remodeling.

    Evidence Affinity labeling and GAG composition analysis in osteoblasts

    PMID:1556106

    Open questions at the time
    • Functional consequences of bFGF–betaglycan interaction for FGF signaling unclear
    • In vivo relevance not tested
  4. 1993 High

    The central co-receptor mechanism was established: membrane betaglycan directly presents TGF-β to the type II signaling receptor in a ternary complex, enhancing cell responsiveness and equalizing isoform-specific differences, while a recombinant ectodomain fragment could enhance TGF-β binding to TGFBR2 at low concentrations.

    Evidence Affinity labeling, cross-linking, cell-based binding, and bioassays; recombinant fragment competition binding

    PMID:8226781 PMID:8391934

    Open questions at the time
    • Stoichiometry and structural basis of ternary complex unknown
    • Mechanism of TGF-β handoff to signaling receptors undefined
  5. 1994 High

    Domain mapping showed TGF-β binds the N-terminal endoglin-related region; GAG attachment sites were identified at Ser535/Ser546 in the uromodulin-related region. Critically, soluble betaglycan cannot present TGF-β and instead acts as a potent inhibitor, particularly of TGF-β2, establishing soluble betaglycan as a natural antagonist.

    Evidence Site-directed and deletion mutagenesis with cell-based binding and functional assays; plasmin cleavage releasing TGF-β–betaglycan complexes from cells

    PMID:8068006 PMID:8106553

    Open questions at the time
    • Protease(s) mediating physiological shedding not identified
    • In vivo antagonist function of soluble betaglycan unconfirmed
  6. 2000 High

    A second major co-receptor function was discovered: betaglycan binds inhibin A with high affinity and, together with ActRII, confers inhibin sensitivity to cells, mediating functional antagonism of activin signaling — establishing betaglycan as a bifunctional co-receptor for both TGF-β and inhibin.

    Evidence Receptor binding assays, cross-linking, co-expression, and functional antagonism assays; co-IP showing endoglin–betaglycan complex on endothelial cells

    PMID:10746731 PMID:10951214

    Open questions at the time
    • Inhibin binding domain on betaglycan not mapped
    • Whether inhibin and TGF-β compete for betaglycan unknown
  7. 2001 High

    The ectodomain was shown to contain two independent TGF-β-binding domains — the N-terminal endoglin-related region mediating presentation to TGFBR2 and the C-terminal uromodulin-related region binding both TGF-β2 and inhibin A. Separately, GAG chains were found to inhibit TGF-β signaling by preventing TGFBR1–TGFBR2 complex formation in specific cell contexts.

    Evidence Deletion mutagenesis with Smad2 phosphorylation readouts; GAG-deficient mutants in LLC-PK1 cells with reporter and receptor co-IP assays; recombinant soluble betaglycan characterization by SPR and bioassay

    PMID:11256966 PMID:11278442 PMID:11668175

    Open questions at the time
    • Structural basis of each domain's ligand binding unknown
    • How context determines whether betaglycan promotes or inhibits signaling unresolved
  8. 2002 Medium

    TGF-β and inhibin A were shown to compete for betaglycan binding on gonadotrope cells, with TGF-β reversing inhibin antagonism of activin-induced FSH gene expression, linking the two co-receptor functions through a shared binding surface.

    Evidence Radiolabeled inhibin A competition binding, receptor co-IP, and luciferase reporter in LβT2 cells

    PMID:12456797

    Open questions at the time
    • Molecular basis of competition not resolved at residue level
    • In vivo physiological significance of TGF-β–inhibin competition for betaglycan undetermined
  9. 2003 High

    MT1-MMP was identified as the protease mediating betaglycan ectodomain shedding, generating a 90 kDa soluble fragment retaining TGF-β2-preferential binding, providing a mechanism for regulated production of the soluble antagonist form.

    Evidence Overexpression of MT-MMPs in COS-1 cells with metalloprotease inhibitors and binding competition

    PMID:14672946

    Open questions at the time
    • Physiological stimuli triggering shedding in vivo not identified
    • Fate of remaining transmembrane fragment not explored
  10. 2006 High

    The inhibin-binding site was mapped to residues 591–700 within the ZP domain, with Val614 critical for inhibin but not TGF-β binding, enabling functional separation of inhibin co-receptor and TGF-β presentation activities. Separately, betaglycan was found to signal independently of TGF-β ligand through p38 MAPK via its cytoplasmic domain.

    Evidence Point mutagenesis (V614Y) with binding and functional reporter assays; adenoviral overexpression with p38 inhibitor and TGF-β blocking antibodies

    PMID:16413747 PMID:16621788

    Open questions at the time
    • Structural basis of ZP domain–inhibin interface not resolved
    • Cytoplasmic domain signaling partners for p38 activation unknown
  11. 2008 High

    The reciprocal inhibin epitope for betaglycan binding was mapped to the inhibin α-subunit outer convex surface (Val108–Tyr120), with triple alanine substitution abolishing betaglycan-dependent inhibin suppression of activin-induced FSH release.

    Evidence Site-directed mutagenesis of inhibin A with binding assay and pituitary cell FSH bioassay

    PMID:18397882

    Open questions at the time
    • No co-crystal structure of inhibin–betaglycan complex
    • Whether same epitope mediates inhibin B binding unclear
  12. 2009 High

    In vivo genetic studies established that betaglycan is required for fetal testis development and dose-sensitively controls kidney morphogenesis, while biophysical studies showed that high-affinity TGF-β binding requires both ectodomain lobes tethered together, with plasmin cleavage between them abolishing neutralizing activity. Betaglycan was confirmed as an obligate endogenous inhibin co-receptor in primary gonadotropes.

    Evidence Knockout/heterozygous mice with morphological and molecular phenotyping; plasmin proteolysis with SPR and bioassay; siRNA and neutralizing antibody in primary gonadotropes

    PMID:19372236 PMID:19696014 PMID:19842711 PMID:21533152

    Open questions at the time
    • Embryonic lethality of null mice limits adult phenotype analysis
    • Whether developmental phenotypes are TGF-β-, inhibin-, or Wnt-dependent unresolved
  13. 2010 Medium

    Inhibin A was found to antagonize TGF-β2 signaling by inducing clathrin-independent endocytic internalization of betaglycan, reducing surface TGF-β2 binding sites — a mechanism distinct from TGF-β-induced internalization. The transmembrane-cytoplasmic stub remaining after shedding was identified as a γ-secretase substrate whose accumulation blunts TGF-β2 signaling.

    Evidence Endocytosis inhibitors and binding assays in adrenocortical cells; γ-secretase inhibitors and reporter assays in HepG2 cells

    PMID:20160125 PMID:21167215

    Open questions at the time
    • Downstream fate of γ-secretase-released intracellular domain unknown
    • Whether internalized betaglycan is recycled or degraded unclear
  14. 2011 High

    The crystal structure of the betaglycan ZP-C domain at 2.0 Å revealed an immunoglobulin-like fold with a convex surface pocket important for TGF-β binding, and explained why betaglycan, lacking the ZP maturation cleavage site, does not polymerize like other ZP proteins.

    Evidence X-ray crystallography at 2.0 Å resolution

    PMID:21402931

    Open questions at the time
    • No structure of full ectodomain or ternary ligand–receptor complex
    • ZP-C–inhibin binding interface not structurally resolved
  15. 2013 High

    Betaglycan was shown to act as a signaling switch that redirects TGF-β signaling from Smad2/3 toward Smad1/5/8 via ALK1, driving myofibroblast differentiation in lung fibroblasts, with expression upregulated by glucocorticoids.

    Evidence Dexamethasone treatment, siRNA, reporter assays, and in vivo mouse lung experiments

    PMID:24347165

    Open questions at the time
    • Mechanism of ALK1 pathway potentiation by betaglycan unclear
    • Whether this switch operates in other fibroblast lineages unknown
  16. 2014 Medium

    TGFBR3 was found to scaffold a complex with β-arrestin 2 and IκBα to inhibit NF-κB signaling, suppressing EMT and migration in oral cancer cells — a TGF-β-independent signaling mechanism mediated by its cytoplasmic domain.

    Evidence Co-immunoprecipitation, overexpression, β-arrestin 2 siRNA, migration/invasion assays

    PMID:29130787

    Open questions at the time
    • Direct binding between TGFBR3 cytoplasmic domain and β-arrestin 2 not demonstrated with purified proteins
    • Physiological trigger for this complex formation unknown
  17. 2016 High

    Biophysical studies defined the hand-off mechanism quantitatively: betaglycan binds TGF-β homodimer with 1:1 stoichiometry allowing one TGFBR2 to bind simultaneously, but betaglycan must be displaced for TGFBR1 recruitment. Separately, betaglycan GAG chains were shown to independently regulate Wnt3a signaling, with heparan sulfate and chondroitin sulfate exerting opposing effects.

    Evidence SPR, ITC, and SEC for stoichiometry; GAG mutant constructs with Wnt reporter assays

    PMID:27784788 PMID:27951653

    Open questions at the time
    • Whether hand-off occurs on the plasma membrane in real time not visualized
    • In vivo relevance of GAG-mediated Wnt regulation not tested
  18. 2018 High

    NMR and mutagenesis mapped the betaglycan ZP-C binding site on TGF-β2 to the inner concave finger region (Ile-92, Lys-97, Glu-99), explaining isoform selectivity for TGF-βs and inhibin A over BMPs. Conditional gonadotrope knockout confirmed TGFBR3 as an inhibin A-specific (not inhibin B) co-receptor in vivo, with knockout females showing super-fertility.

    Evidence NMR titrations, SPR, site-directed mutagenesis; conditional Cre-lox gonadotrope knockout with FSH assays

    PMID:30364975 PMID:30598510

    Open questions at the time
    • Full-length betaglycan–TGF-β2 co-structure still lacking at this point
    • Mechanism of inhibin A vs. inhibin B selectivity at structural level unresolved
  19. 2025 High

    Cryo-EM structure of TGF-β bound simultaneously to betaglycan and TGFBR1/TGFBR2 provided near-atomic resolution of the hand-off mechanism, revealing how betaglycan engages TGF-β at interfaces distinct from endoglin and is displaced upon signaling receptor assembly.

    Evidence Cryo-EM structural determination with functional validation

    PMID:40011426

    Open questions at the time
    • Structure of betaglycan–inhibin–ActRII ternary complex not yet determined
    • Role of GAG chains in the structural assembly not visualized

Open questions

Synthesis pass · forward-looking unresolved questions
  • Key unresolved questions include the structural basis of the inhibin A–betaglycan–ActRII ternary complex, the identity of cytoplasmic domain binding partners mediating p38 MAPK and β-arrestin 2 signaling, the physiological contexts governing whether betaglycan promotes versus inhibits TGF-β signaling, and the in vivo significance of GAG-mediated Wnt regulation.
  • No structure of inhibin–betaglycan–ActRII complex
  • Cytoplasmic domain signaling partners not identified by unbiased approaches
  • Context-dependent switch between positive and negative TGF-β regulation not mechanistically resolved

Mechanism profile

Synthesis pass · controlled-vocabulary classification · explore literature graph →
Molecular activity
GO:0060089 molecular transducer activity 4 GO:0060090 molecular adaptor activity 4 GO:0098772 molecular function regulator activity 4 GO:0048018 receptor ligand activity 2
Localization
GO:0005576 extracellular region 4 GO:0005886 plasma membrane 4
Pathway
R-HSA-162582 Signal Transduction 7 R-HSA-1266738 Developmental Biology 2 R-HSA-1474165 Reproduction 2
Partners
ACVR2AARRB2ENGGIPC1INHAMMP14TGFBR1TGFBR2
Complex memberships
Betaglycan–endoglin complexBetaglycan–β-arrestin 2–IκBα complexInhibin A–betaglycan–ActRII ternary complexTGF-β–betaglycan–TGFBR2 ternary complex

Evidence

Reading pass · 42 per-paper findings extracted from the source corpus
Year Finding Method Journal Conf PMIDs
1993 Betaglycan (TGFBR3) presents TGF-β directly to the type II signaling receptor kinase, forming a high-affinity ternary complex. Membrane betaglycan increases TGF-β binding to the signaling receptor, enhances cell responsiveness to TGF-β, and eliminates biological differences between TGF-β isoforms. Affinity labeling, cross-linking, cell-based binding assays, bioassays Cell High 8391934
1991 Betaglycan is a membrane-anchored proteoglycan with an extracellular domain carrying glycosaminoglycan chains; its ectodomain can be shed as a soluble proteoglycan. The transmembrane and cytoplasmic regions share homology with endoglin. GAG chains are dispensable for TGF-β binding to the core protein. cDNA cloning, structural analysis, biochemical characterization Cell High 1657406
1989 Betaglycan exists in both membrane-bound and soluble forms; the membrane form is hydrophobic and associates with liposomes, while soluble forms lack a membrane anchor. Both bind TGF-β via the core protein and carry heparan sulfate and/or chondroitin sulfate GAG chains. Affinity labeling, liposome association assay, biochemical fractionation The Journal of cell biology High 2592419
1994 TGF-β binds to the NH2-terminal endoglin-related region of betaglycan. GAG attachment sites are Ser535 and Ser546 in the uromodulin-related region; their mutation prevents GAG attachment but does not affect TGF-β binding or presentation. Soluble betaglycan (lacking membrane anchor) cannot present TGF-β to the type II receptor and instead acts as a potent inhibitor of TGF-β, particularly the TGF-β2 isoform. Site-directed mutagenesis, deletion mutagenesis, cell-based binding assays The Journal of cell biology High 8106553
2000 Betaglycan functions as an inhibin co-receptor with ActRII. Betaglycan binds inhibin with high affinity, enhances inhibin binding in cells co-expressing ActRII and betaglycan, and inhibin forms crosslinked complexes with both betaglycan and ActRII. Betaglycan confers inhibin sensitivity to cell lines that otherwise respond poorly, mediating functional antagonism of activin signaling. Receptor binding assays, cross-linking, co-expression, functional antagonism assays Nature High 10746731
1992 Betaglycan binds bFGF via its heparan sulfate chains (separate from the TGF-β binding core protein domain). bFGF treatment of osteoblasts selectively reduces heparan sulfate GAG content of betaglycan without affecting chondroitin sulfate or core protein, demonstrating ligand-regulated remodeling of the bFGF-binding domain. Affinity labeling, GAG composition analysis, cell-based ligand binding The Journal of biological chemistry High 1556106
2001 Betaglycan ectodomain contains two independent TGF-β binding domains: the NH2-terminal endoglin-related region and the COOH-terminal uromodulin-related region. Only the endoglin-related region mediates TGF-β presentation to TGF-β type II receptor. The uromodulin-related region specifically binds inhibin A with relative affinities TGF-β2 > inhibin A > TGF-β1. Deletion mutagenesis, ligand binding competition, Smad2 phosphorylation assays The Journal of biological chemistry High 11278442
2001 Recombinant soluble betaglycan is a homodimer (two 110 kDa monomers, non-covalent) lacking GAG chains. It binds TGF-β isoforms with relative affinities TGF-β2 > TGF-β3 > TGF-β1, with Kd ~3.5 nM for TGF-β1, and neutralizes TGF-β activity with 10-fold higher potency against TGF-β2 than TGF-β1. Baculovirus expression, biochemical characterization, bioassay The Biochemical journal High 11256966
2001 In LLC-PK1 renal epithelial cells (which lack endogenous betaglycan), expressed betaglycan inhibits TGF-β signaling by preventing type I–type II receptor complex formation, not by ligand sequestration. This inhibitory effect is mediated by the glycosaminoglycan modifications; a GAG-deficient betaglycan mutant does not inhibit signaling or receptor association. Reporter gene assay, thymidine incorporation, Smad2/3 phosphorylation, co-immunoprecipitation of receptor complexes, GAG mutant The Journal of biological chemistry High 11668175
2003 Betaglycan shedding (release of the soluble ectodomain) is induced by pervanadate (a tyrosine phosphatase inhibitor) and generates a 90 kDa fragment (sBG-90) whose production is mediated by MT1-MMP (membrane type-1 matrix metalloprotease). MT3-MMP can also generate this fragment. The released sBG-90 retains preferential binding to TGF-β2 over TGF-β1. Overexpression of MT-MMPs in COS-1 cells, metalloprotease inhibitors, binding competition The Journal of biological chemistry High 14672946
1993 A fragment of betaglycan ectodomain (amino acids 543–769) near the transmembrane domain binds TGF-β and at low concentrations enhances TGF-β binding to the type II receptor. The same site is competed by decorin, biglycan, and fibromodulin, indicating overlapping binding interfaces in TGF-β. Recombinant fusion protein expression, competition binding assay, affinity cross-linking, bioassay The Journal of biological chemistry High 8226781
2006 Betaglycan domain spanning amino acids 591–700 (within the ZP domain) is the only inhibin-binding region. The inhibin and TGF-β binding residues overlap; Val614Tyr mutation abolishes inhibin binding but retains TGF-β binding via the N-terminal site. Betaglycan V614Y mutants fail to mediate inhibin antagonism of activin signaling but can still present TGF-β to TβRII, functionally separating the two co-receptor activities. Deletion and point mutagenesis, ligand binding assays, functional antagonism reporter assays The Journal of biological chemistry High 16621788
2006 Betaglycan can signal in a TGF-β ligand-independent manner through activation of the p38 MAPK pathway, requiring its cytoplasmic domain. This effect increases TGF-β target gene expression (fibronectin, CTGF) and inhibits myogenin in myoblasts independently of Smad2 phosphorylation. Adenoviral overexpression, reporter assays, TGF-β blocking antibodies, p38 inhibitor, cytoplasmic domain mutant Cellular signalling Medium 16413747
2009 Betaglycan ectodomain has a bilobular structure; each lobe folds independently and binds TGF-β through distinct non-overlapping interfaces. High-affinity TGF-β binding (Kd low nanomolar) requires both domains tethered together; individual domains bind 1–2 orders of magnitude more weakly. Plasmin cleaves betaglycan between the two domains, separating them and abolishing neutralizing activity. Plasmin proteolysis, N-terminal sequencing, surface plasmon resonance, TGF-β activity bioassay Biochemistry High 19842711
2011 Crystal structure of the betaglycan ZP-C domain (2.0 Å resolution) reveals an immunoglobulin-like fold. The external hydrophobic patch is integral to ZP-C (corresponds to ZP-C G strand). The AB loop and convex surface pocket are important for TGF-β ligand binding. Absence of the maturation cleavage site (present in polymerizing ZP proteins) explains why betaglycan does not polymerize. X-ray crystallography at 2.0 Å resolution Proceedings of the National Academy of Sciences of the United States of America High 21402931
2016 Betaglycan binds TGF-β homodimers with 1:1 stoichiometry allowing one TβRII to bind simultaneously. Betaglycan modestly potentiates TβRII binding to TGF-β2 but must be displaced for TβRI to bind. This defines a hand-off mechanism: betaglycan concentrates TGF-β2 on the cell surface, promotes TβRII binding by membrane-localization and allostery, and is subsequently displaced by TβRI recruitment. Surface plasmon resonance, isothermal titration calorimetry, size-exclusion chromatography Biochemistry High 27951653
2018 NMR titrations and SPR identified the BGZP-C binding site on TGF-β2 as the inner concave surface of its extended finger region, involving residues Ile-92, Lys-97, and Glu-99 specific to TGF-β isoforms and inhibin-α. Mutation of these residues to the BMP-2 equivalents reduces BGZP-C binding, explaining betaglycan selectivity for TGF-βs and inhibin A over BMPs. NMR (methyl-labeled TGF-β2), surface plasmon resonance, site-directed mutagenesis The Journal of biological chemistry High 30598510
2025 Cryo-EM/structural determination of TGF-β bound simultaneously to betaglycan and the signaling receptors TGFBR1 and TGFBR2 reveals key ligand engagement interfaces distinct from those of endoglin. The structure explains the hand-off mechanism: betaglycan binds TGF-β, facilitates signaling receptor assembly, then is displaced as signaling receptors engage. Cryo-EM/structural biology with functional validation Nature communications High 40011426
2013 Glucocorticoids (dexamethasone) upregulate Tgfbr3 expression in lung fibroblasts, and Tgfbr3 functions as a signaling switch that blunts Tgfbr1/Smad2/3 signaling while potentiating Acvrl1/Smad1/5/8 signaling, driving TGF-β-dependent myofibroblast differentiation (smooth muscle actin and myosin acquisition) in a Smad1-dependent manner. Dexamethasone treatment, siRNA knockdown, reporter assays, in vivo mouse lung experiments The Journal of biological chemistry High 24347165
2010 Inhibin-A antagonizes TGFβ2 signaling by inducing clathrin-independent endocytic internalization of betaglycan, reducing available cell-surface betaglycan binding sites for TGFβ2. This is distinct from TGFβ-induced betaglycan internalization and depends on mutual affinity of inhibin-A and TGFβ2 for betaglycan. Cell-surface binding assay, endocytosis inhibitors, functional signaling assays in adrenocortical cells Molecular endocrinology Medium 20160125
2009 Betaglycan is an endogenous obligate co-receptor for high-potency inhibin antagonism of activin signaling in rat anterior pituitary gonadotropes. RNAi knockdown and immunoneutralization of betaglycan each independently reduce the potency of inhibin-A antagonism of activin-induced FSH secretion by >1000-fold. siRNA knockdown, neutralizing antibody, primary gonadotrope cultures, FSH secretion assay Molecular endocrinology High 19372236
2018 Conditional knockout of Tgfbr3 specifically in murine gonadotropes impairs inhibin A (but not inhibin B) suppression of FSH synthesis in cultured pituitaries, demonstrating that TGFBR3 is an inhibin A-specific co-receptor in vivo in gonadotropes. Conditional knockout females are super-fertile with enhanced folliculogenesis. Conditional knockout mouse model (gonadotrope-specific Cre), FSH secretion assay, pituitary culture Endocrinology High 30364975
1994 Plasmin selectively cleaves betaglycan on intact cells, releasing a 60 kDa TGF-β-betaglycan complex into the medium. The type I and type II TGF-β receptors are not plasmin substrates. Plasmin-treated cells release more active TGF-β, indicating betaglycan cleavage liberates active growth factor. Affinity labeling, SDS-PAGE of cell surface receptors, TGF-β bioassay The Biochemical journal Medium 8068006
2012 Granzyme B cleaves soluble betaglycan (along with decorin and biglycan) and releases active TGF-β1 from these proteoglycans. The released TGF-β1 retains activity, inducing SMAD-3 phosphorylation in human coronary artery smooth muscle cells. In vitro cleavage assay, cytokine release assay, SMAD3 phosphorylation, granzyme B inhibitor PloS one Medium 22479366
2000 On human microvascular endothelial cells, endoglin associates with betaglycan in a complex that can form in a ligand-dependent or ligand-independent manner. Three higher-order complexes containing endoglin with type I and/or type II TGF-β receptors are also present. Co-immunoprecipitation, affinity labeling with radiolabeled TGF-β European journal of biochemistry Medium 10951214
2003 On human chondrocytes, endoglin forms a heteromeric complex with betaglycan in both a ligand-independent and ligand-dependent manner, independent of the type II TGF-β receptor, as shown by co-immunoprecipitation at endogenous receptor concentrations. Co-immunoprecipitation, affinity labeling with radiolabeled TGF-β Journal of bone and mineral research Medium 12568406
1998 Betaglycan overexpression in rat myoblasts enhances TGF-β inhibition of proliferation and PAI-1 synthesis, and specifically increases TGF-β binding to the type II receptor (~3.5-fold). Endoglin overexpression has weaker and distinct effects (increases binding to both type I and II receptors). The differential effects reside in the extracellular domain, shown by chimeric protein analysis. Overexpression, 125I-TGF-β affinity cross-linking, proliferation assay, chimeric protein analysis The Journal of biological chemistry Medium 9830054
2010 Betaglycan's transmembrane-cytoplasmic fragment remaining after ectodomain shedding is stable in cells and is a substrate of γ-secretase. γ-Secretase inhibition or expression of the transmembrane-cytoplasmic fragment blunts TGF-β2 signaling in HepG2 cells. γ-Secretase inhibitors, shedding inhibitor TAPI-2, transfection, TGF-β signaling reporter Biochimica et biophysica acta Medium 21167215
2009 Tgfbr3 (betaglycan) knockout mice show defective seminiferous cord formation, reduced fetal Leydig cell function (decreased Insl3, Cyp17a1, Cyp11a1, Star, Hsd3b1 expression), and reduced Sertoli cell markers (Dhh, Sox9, Amh) without changes in Leydig cell number, indicating betaglycan is required for normal fetal testis structure and endocrine function. Knockout mouse model, immunohistochemistry, quantitative RT-PCR, whole-mount in situ hybridization, morphometry Biology of reproduction High 19696014
2011 Betaglycan heterozygous knockout mice have augmented nephron number and accelerated ureteric branching, while null mice show renal hypoplasia and reduced nephron number. Opposing molecular phenotypes involve altered expression of Bmp4, Pax2, Gdnf, Ret, Wnt4 and other metanephric regulatory genes, demonstrating dose-sensitive betaglycan requirement for kidney development. Knockout and heterozygous mouse models, stereological nephron counting, quantitative RT-PCR PloS one High 21533152
2016 TGFBR3/betaglycan, independent of its TGF-β co-receptor function, regulates canonical Wnt3a signaling through its GAG chains: heparan sulfate chains sequester Wnt3a and inhibit Wnt signaling, while chondroitin sulfate chains promote Wnt3a signaling. The two GAG modifications have opposing effects on Wnt availability. GAG mutant constructs, Wnt reporter assays, ligand binding experiments The Journal of biological chemistry Medium 27784788
2008 The inhibin A binding site on betaglycan maps to an epitope on the outer convex surface of the inhibin α-subunit (residues Val108–Tyr120). Simultaneous substitution of Thr111, Ser112, and Tyr120 to alanine abolishes betaglycan binding and prevents inhibin A suppression of activin-induced FSH release from rat pituitary cells. Site-directed mutagenesis of inhibin A, binding assay, pituitary cell bioassay The Journal of biological chemistry High 18397882
2007 Loss of betaglycan expression in ovarian cancer cells is partly due to epigenetic silencing (reversed by 5-aza-2'-deoxycytidine and trichostatin A combination). Restoring betaglycan in Ovca429 cells inhibits cancer cell motility and invasiveness, and enhances antimigratory effects of inhibin and inhibin-mediated repression of MMP levels. Epigenetic drug treatment, stable transfection, motility/invasion assays, MMP measurement Cancer research Medium 17522389
2014 TGFBR3 forms a complex with β-arrestin 2 scaffolding protein and IκBα. Overexpression of TGFBR3 decreases p-p65 and increases IκBα expression, inhibiting NF-κB signaling; this effect is abolished by β-arrestin 2 knockdown. This pathway inhibits EMT and migration in oral squamous cell carcinoma cells. Co-immunoprecipitation, overexpression, siRNA knockdown, migration/invasion assays Cell adhesion & migration Medium 29130787
2019 TGFBR3 induces secretion of angiogenin (ANG), and ANG is required and sufficient to mediate TGFBR3-dependent inhibition of migration and invasion in SMAD4-positive oral cancer cells. In SMAD4-deficient cells, TGFBR3 suppression requires GIPC1 (but not ARRB2), indicating SMAD4-dependent and -independent mechanisms. Overexpression, KD of ARRB2/GIPC1, migration/invasion assays, SMAD4-null cell comparison Cancers Medium 32471132
2018 Loss of TGFBR3 in clear-cell renal cell carcinoma increases ALDH-positive cancer-initiating cell populations (TGF-β-dependent), and independently enhances cell migration via FAK-PI3K signaling with increased lamellipodium formation, demonstrating TGF-β-dependent and TGF-β-independent metastatic mechanisms of TGFBR3. Orthotopic inoculation in mice, ALDH flow cytometry, FAK-PI3K inhibitors, migration assay, stable KD Oncogene Medium 29391598
2014 Lactoferrin directly interacts with betaglycan (TGFBR3) and induces formation of the TGFBR3/TβRII/TβRI complex, leading to Smad3 phosphorylation and IgA isotype switching in B cells. Retinoic acid further augments this by increasing betaglycan expression. Direct binding assay, co-immunoprecipitation of receptor complex, Smad3 phosphorylation, IgA reporter assay, in vivo peroral administration Mucosal immunology Medium 25492477
2019 Betaglycan loss in mesenchymal stromal cells augments TGF-β signaling, proliferation, and migration, and completely blocks osteoblast differentiation. Betaglycan controls expression of Wnt5a (>60-fold increase upon loss), which activates canonical Wnt signaling to impair osteogenesis. A Wnt5a neutralizing antibody rescues osteogenic gene expression in betaglycan-ablated MSCs. siRNA knockdown, recombinant Wnt5a addition, neutralizing antibody, osteogenic differentiation assay, in vivo xenograft model Oncogene Medium 31409900
2019 TGFBR3 is identified as a target of let-7 microRNA. Induction of Tgfbr3 in cardiomyocytes causes apoptosis through p38 MAPK activation. In vivo AAV9-mediated let-7 knockdown exacerbates cardiomyocyte apoptosis after myocardial infarction, while let-7 overexpression reduces it. AAV9-mediated microRNA overexpression/knockdown in mice, apoptosis assays, p38 MAPK measurement EBioMedicine Medium 31401194
2002 TGF-β competes with inhibin A for binding to betaglycan on gonadotrope LβT2 cells, thereby reversing inhibin A antagonism of activin-induced FSHβ and GnRHR promoter activity. Immunoprecipitation confirmed TGF-β1 and TGF-β2 compete with inhibin A for betaglycan binding. Radiolabeled inhibin A competition binding, co-immunoprecipitation of receptor complexes, luciferase reporter assay Molecular endocrinology Medium 12456797
2002 Betaglycan promoter is regulated by MyoD (but not myogenin) and retinoic acid (upregulation) and by TGF-β isoforms (downregulation). Betaglycan expression is upregulated during C2C12 myoblast-to-myotube differentiation, and forced betaglycan expression increases TGF-β2 responsiveness in myoblasts. Northern/Western blot during differentiation, promoter cloning and reporter assay, transcription factor overexpression, affinity labeling, immunofluorescence The Journal of biological chemistry Medium 12399463
2011 TGFBR3 overexpression in cardiac fibroblasts prevents hypoxia-induced apoptosis by attenuating TGF-β1/p-Smad2/3 signaling, blocking TGFBR1-TGFBR2 complex formation, reversing Bax upregulation and Bcl-2 downregulation, and inhibiting hypoxia-induced calcium influx. Overexpression, MTT assay, TUNEL, co-immunoprecipitation of receptor complex, calcium imaging Journal of cellular physiology Medium 21792916

Source papers

Stage 0 corpus · 100 papers · ranked by NIH iCite citations
Year Title Journal Citations PMID
1993 Betaglycan presents ligand to the TGF beta signaling receptor. Cell 814 8391934
1991 Structure and expression of the membrane proteoglycan betaglycan, a component of the TGF-beta receptor system. Cell 613 1657406
2000 Betaglycan binds inhibin and can mediate functional antagonism of activin signalling. Nature 476 10746731
1994 Betaglycan can act as a dual modulator of TGF-beta access to signaling receptors: mapping of ligand binding and GAG attachment sites. The Journal of cell biology 349 8106553
1989 Membrane-anchored and soluble forms of betaglycan, a polymorphic proteoglycan that binds transforming growth factor-beta. The Journal of cell biology 334 2592419
2019 Macrophage-derived exosomal microRNA-501-3p promotes progression of pancreatic ductal adenocarcinoma through the TGFBR3-mediated TGF-β signaling pathway. Journal of experimental & clinical cancer research : CR 277 31307515
1998 Role of endoglin in cellular responses to transforming growth factor-beta. A comparative study with betaglycan. The Journal of biological chemistry 192 9830054
2009 Genome-wide association and follow-up replication studies identified ADAMTS18 and TGFBR3 as bone mass candidate genes in different ethnic groups. American journal of human genetics 155 19249006
2001 Ligand binding and functional properties of betaglycan, a co-receptor of the transforming growth factor-beta superfamily. Specialized binding regions for transforming growth factor-beta and inhibin A. The Journal of biological chemistry 134 11278442
1992 Binding of two growth factor families to separate domains of the proteoglycan betaglycan. The Journal of biological chemistry 127 1556106
2002 Antitumor activity of a recombinant soluble betaglycan in human breast cancer xenograft. Cancer research 124 12183427
2001 Betaglycan inhibits TGF-beta signaling by preventing type I-type II receptor complex formation. Glycosaminoglycan modifications alter betaglycan function. The Journal of biological chemistry 115 11668175
2003 The shedding of betaglycan is regulated by pervanadate and mediated by membrane type matrix metalloprotease-1. The Journal of biological chemistry 105 14672946
2011 Consistent t(1;10) with rearrangements of TGFBR3 and MGEA5 in both myxoinflammatory fibroblastic sarcoma and hemosiderotic fibrolipomatous tumor. Genes, chromosomes & cancer 99 21717526
2007 Loss of betaglycan expression in ovarian cancer: role in motility and invasion. Cancer research 99 17522389
2012 Granzyme B cleaves decorin, biglycan and soluble betaglycan, releasing active transforming growth factor-β1. PloS one 95 22479366
2011 Betaglycan: a multifunctional accessory. Molecular and cellular endocrinology 93 21550381
2002 Expression of activin receptors, follistatin and betaglycan by human endometrial stromal cells; consistent with a role for activins during decidualization. Molecular human reproduction 84 11912285
2018 Upregulated lncRNA ADAMTS9-AS2 suppresses progression of lung cancer through inhibition of miR-223-3p and promotion of TGFBR3. IUBMB life 78 29707897
2001 Recombinant soluble betaglycan is a potent and isoform-selective transforming growth factor-beta neutralizing agent. The Biochemical journal 78 11256966
2011 Genome-wide association studies in Asians confirm the involvement of ATOH7 and TGFBR3, and further identify CARD10 as a novel locus influencing optic disc area. Human molecular genetics 70 21307088
2011 TGFBR3, a potential negative regulator of TGF-β signaling, protects cardiac fibroblasts from hypoxia-induced apoptosis. Journal of cellular physiology 70 21792916
2002 Properties of inhibin binding to betaglycan, InhBP/p120 and the activin type II receptors. Molecular and cellular endocrinology 70 12385827
2006 Identification of distinct inhibin and transforming growth factor beta-binding sites on betaglycan: functional separation of betaglycan co-receptor actions. The Journal of biological chemistry 69 16621788
2000 Endoglin expression on human microvascular endothelial cells association with betaglycan and formation of higher order complexes with TGF-beta signalling receptors. European journal of biochemistry 68 10951214
2014 A time- and matrix-dependent TGFBR3-JUND-KRT5 regulatory circuit in single breast epithelial cells and basal-like premalignancies. Nature cell biology 65 24658685
2005 Systemic administration of a soluble betaglycan suppresses tumor growth, angiogenesis, and matrix metalloproteinase-9 expression in a human xenograft model of prostate cancer. The Prostate 60 15468171
1993 Localization of transforming growth factor beta binding site in betaglycan. Comparison with small extracellular matrix proteoglycans. The Journal of biological chemistry 60 8226781
2018 Decreased TGFBR3/betaglycan expression enhances the metastatic abilities of renal cell carcinoma cells through TGF-β-dependent and -independent mechanisms. Oncogene 59 29391598
2020 Regulation of H2S-induced necroptosis and inflammation in broiler bursa of Fabricius by the miR-15b-5p/TGFBR3 axis and the involvement of oxidative stress in this process. Journal of hazardous materials 58 33307448
2014 TGFBR3 and MGEA5 rearrangements in pleomorphic hyalinizing angiectatic tumors and the spectrum of related neoplasms. The American journal of surgical pathology 58 24705316
2002 The distribution of betaglycan protein and mRNA in rat brain, pituitary, and gonads: implications for a role for betaglycan in inhibin-mediated reproductive functions. Endocrinology 58 11861534
2013 Glucocorticoids recruit Tgfbr3 and Smad1 to shift transforming growth factor-β signaling from the Tgfbr1/Smad2/3 axis to the Acvrl1/Smad1 axis in lung fibroblasts. The Journal of biological chemistry 57 24347165
2002 Expression and localization of inhibin alpha, inhibin/activin betaA and betaB and the activin type II and inhibin beta-glycan receptors in the developing human testis. Reproduction (Cambridge, England) 57 12052232
2009 Fetal testis dysgenesis and compromised Leydig cell function in Tgfbr3 (beta glycan) knockout mice. Biology of reproduction 56 19696014
1991 Purification of the transforming growth factor-beta (TGF-beta) binding proteoglycan betaglycan. The Journal of biological chemistry 56 1744125
2010 Changes in expression of bone morphogenetic proteins (BMPs), their receptors and inhibin co-receptor betaglycan during bovine antral follicle development: inhibin can antagonize the suppressive effect of BMPs on thecal androgen production. Reproduction (Cambridge, England) 55 20739376
2007 TGFBR3 loss and consequences in prostate cancer. The Prostate 55 17192875
2019 Structural biology of betaglycan and endoglin, membrane-bound co-receptors of the TGF-beta family. Experimental biology and medicine (Maywood, N.J.) 51 31601110
2021 Transforming Growth Factor Beta Receptor 3 (TGFBR3)-Associated Membranous Nephropathy. Kidney360 49 35369660
1992 Subtypes of betaglycan and of type I and type II transforming growth factor-beta (TGF-beta) receptors with different affinities for TGF-beta 1 and TGF-beta 2 are exhibited by human placental trophoblast cells. Journal of cellular physiology 49 1310325
2006 Soluble betaglycan reduces renal damage progression in db/db mice. American journal of physiology. Renal physiology 48 16954341
2009 Loss of betaglycan contributes to the malignant properties of human granulosa tumor cells. Molecular endocrinology (Baltimore, Md.) 47 19164448
2011 Structure of betaglycan zona pellucida (ZP)-C domain provides insights into ZP-mediated protein polymerization and TGF-beta binding. Proceedings of the National Academy of Sciences of the United States of America 45 21402931
2019 Novel role of the clustered miR-23b-3p and miR-27b-3p in enhanced expression of fibrosis-associated genes by targeting TGFBR3 in atrial fibroblasts. Journal of cellular and molecular medicine 43 30729664
2018 Betaglycan (TGFBR3) Functions as an Inhibin A, but Not Inhibin B, Coreceptor in Pituitary Gonadotrope Cells in Mice. Endocrinology 43 30364975
2003 Betaglycan localization in the female rat pituitary: implications for the regulation of follicle-stimulating hormone by inhibin. Endocrinology 43 14500575
2002 Inhibin binding protein (InhBP/p120), betaglycan, and the continuing search for the inhibin receptor. Molecular endocrinology (Baltimore, Md.) 43 11818494
2002 Antagonism of activin by inhibin and inhibin receptors: a functional role for betaglycan. Molecular and cellular endocrinology 42 11911962
2002 Betaglycan expression is transcriptionally up-regulated during skeletal muscle differentiation. Cloning of murine betaglycan gene promoter and its modulation by MyoD, retinoic acid, and transforming growth factor-beta. The Journal of biological chemistry 40 12399463
2020 The STAT3-miR-223-TGFBR3/HMGCS1 axis modulates the progression of cervical carcinoma. Molecular oncology 39 32491253
2016 Binding Properties of the Transforming Growth Factor-β Coreceptor Betaglycan: Proposed Mechanism for Potentiation of Receptor Complex Assembly and Signaling. Biochemistry 39 27951653
2009 Betaglycan has two independent domains required for high affinity TGF-beta binding: proteolytic cleavage separates the domains and inactivates the neutralizing activity of the soluble receptor. Biochemistry 39 19842711
2008 Suppression of inhibin A biological activity by alterations in the binding site for betaglycan. The Journal of biological chemistry 39 18397882
2006 Betaglycan induces TGF-beta signaling in a ligand-independent manner, through activation of the p38 pathway. Cellular signalling 39 16413747
1994 Plasmin cleaves betaglycan and releases a 60 kDa transforming growth factor-beta complex from the cell surface. The Biochemical journal 39 8068006
2019 MicroRNA let-7-TGFBR3 signalling regulates cardiomyocyte apoptosis after infarction. EBioMedicine 38 31401194
2017 miR-19a and miR-424 target TGFBR3 to promote epithelial-to-mesenchymal transition and migration of tongue squamous cell carcinoma cells. Cell adhesion & migration 38 29130787
2009 Endogenous betaglycan is essential for high-potency inhibin antagonism in gonadotropes. Molecular endocrinology (Baltimore, Md.) 38 19372236
2005 Inhibin alpha-subunit and the inhibin coreceptor betaglycan are downregulated in endometrial carcinoma. European journal of endocrinology 38 15745937
2003 Endoglin is expressed on human chondrocytes and forms a heteromeric complex with betaglycan in a ligand and type II TGFbeta receptor independent manner. Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research 38 12568406
2007 Differential expression of TGFBR3 (betaglycan) in mouse ovary and testis during gonadogenesis. Growth factors (Chur, Switzerland) 37 18236212
2010 Inhibin-A antagonizes TGFbeta2 signaling by down-regulating cell surface expression of the TGFbeta coreceptor betaglycan. Molecular endocrinology (Baltimore, Md.) 36 20160125
1996 Betaglycan has multiple binding sites for transforming growth factor-beta 1. The Biochemical journal 36 8645162
2014 Lactoferrin causes IgA and IgG2b isotype switching through betaglycan binding and activation of canonical TGF-β signaling. Mucosal immunology 35 25492477
2023 Exosome-derived circ_0001785 delays atherogenesis through the ceRNA network mechanism of miR-513a-5p/TGFBR3. Journal of nanobiotechnology 34 37794449
2019 Hsa_circ_0042666 inhibits proliferation and invasion via regulating miR-223/TGFBR3 axis in laryngeal squamous cell carcinoma. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie 33 31525642
2002 Transforming growth factor-beta modulates inhibin A bioactivity in the LbetaT2 gonadotrope cell line by competing for binding to betaglycan. Molecular endocrinology (Baltimore, Md.) 32 12456797
2021 Inhibiting microRNA-424 in bone marrow mesenchymal stem cells-derived exosomes suppresses tumor growth in colorectal cancer by upregulating TGFBR3. Archives of biochemistry and biophysics 30 34129838
2007 Alternative splicing of TGF-betas and their high-affinity receptors T beta RI, T beta RII and T beta RIII (betaglycan) reveal new variants in human prostatic cells. BMC genomics 30 17845732
2018 MicroRNA let-7a regulates angiogenesis by targeting TGFBR3 mRNA. Journal of cellular and molecular medicine 29 30467960
2001 Antagonism of activin by inhibin and inhibin receptors: a functional role for betaglycan-glycan. Molecular and cellular endocrinology 29 11451571
1995 Serglycin and betaglycan proteoglycans are expressed in the megakaryocytic cell line CHRF 288-11 and normal human megakaryocytes. Journal of cellular physiology 29 7559813
2020 HELLS, a chromatin remodeler is highly expressed in pancreatic cancer and downregulation of it impairs tumor growth and sensitizes to cisplatin by reexpressing the tumor suppressor TGFBR3. Cancer medicine 28 33280236
2007 Transforming growth factor-beta blocks inhibin binding to different target cell types in a context-dependent manner through dual mechanisms involving betaglycan. Endocrinology 28 17656464
2019 Betaglycan drives the mesenchymal stromal cell osteogenic program and prostate cancer-induced osteogenesis. Oncogene 27 31409900
2018 Plau and Tgfbr3 are YAP-regulated genes that promote keratinocyte proliferation. Cell death & disease 27 30382077
2011 Betaglycan is required for the establishment of nephron endowment in the mouse. PloS one 27 21533152
2023 Exosomal miR-103a-3p from Crohn's Creeping Fat-Derived Adipose-Derived Stem Cells Contributes to Intestinal Fibrosis by Targeting TGFBR3 and Activating Fibroblasts. Journal of Crohn's & colitis 26 36897738
2003 Expression of betaglycan, an inhibin coreceptor, in normal human ovaries and ovarian sex cord-stromal tumors and its regulation in cultured human granulosa-luteal cells. The Journal of clinical endocrinology and metabolism 26 14557487
2013 Betaglycan alters NFκB-TGFβ2 cross talk to reduce survival of human granulosa tumor cells. Molecular endocrinology (Baltimore, Md.) 24 23322721
2016 Altering the Proteoglycan State of Transforming Growth Factor β Type III Receptor (TβRIII)/Betaglycan Modulates Canonical Wnt/β-Catenin Signaling. The Journal of biological chemistry 23 27784788
2020 The Tumor Suppressor TGFBR3 Blocks Lymph Node Metastasis in Head and Neck Cancer. Cancers 22 32471132
2010 The type III TGF-β receptor betaglycan transmembrane-cytoplasmic domain fragment is stable after ectodomain cleavage and is a substrate of the intramembrane protease γ-secretase. Biochimica et biophysica acta 22 21167215
2006 Mutational analysis of the betaglycan gene-coding region in susceptibility for ovarian failure. Human reproduction (Oxford, England) 22 16613887
1999 A regulatory role of fibroblast growth factor in the expression of decorin, biglycan, betaglycan and syndecan in osteoblasts from patients with Crouzon's syndrome. European journal of cell biology 22 10384983
2023 Exosomes Derived from E2F1-/- Adipose-Derived Stem Cells Promote Skin Wound Healing via miR-130b-5p/TGFBR3 Axis. International journal of nanomedicine 21 37941530
2022 LncRNA H19 alleviates sepsis-induced acute lung injury by regulating the miR-107/TGFBR3 axis. BMC pulmonary medicine 21 36180862
2024 Cancer associated fibroblasts-derived SULF1 promotes gastric cancer metastasis and CDDP resistance through the TGFBR3-mediated TGF-β signaling pathway. Cell death discovery 20 38438372
2022 Promoter Hypomethylation of TGFBR3 as a Risk Factor of Alzheimer's Disease: An Integrated Epigenomic-Transcriptomic Analysis. Frontiers in cell and developmental biology 20 35310542
2025 Structures of TGF-β with betaglycan and signaling receptors reveal mechanisms of complex assembly and signaling. Nature communications 19 40011426
2024 The Role of TGFBR3 in the Development of Lung Cancer. Protein and peptide letters 19 39092729
2019 A Tale of Two Proteins: Betaglycan, IGSF1, and the Continuing Search for the Inhibin B Receptor. Trends in endocrinology and metabolism: TEM 19 31648935
2018 TGF-β2 uses the concave surface of its extended finger region to bind betaglycan's ZP domain via three residues specific to TGF-β and inhibin-α. The Journal of biological chemistry 19 30598510
2015 Retinoic acid enhances lactoferrin-induced IgA responses by increasing betaglycan expression. Cellular & molecular immunology 19 26277894
2021 Anti-TGFβ (Transforming Growth Factor β) Therapy With Betaglycan-Derived P144 Peptide Gene Delivery Prevents the Formation of Aortic Aneurysm in a Mouse Model of Marfan Syndrome. Arteriosclerosis, thrombosis, and vascular biology 18 34162229
2018 The t(1;10)(p22;q24) TGFBR3/MGEA5 Translocation in Pleomorphic Hyalinizing Angiectatic Tumor, Myxoinflammatory Fibroblastic Sarcoma, and Hemosiderotic Fibrolipomatous Tumor. Archives of pathology & laboratory medicine 18 29979612
2014 Betaglycan blocks metastatic behaviors in human granulosa cell tumors by suppressing NFκB-mediated induction of MMP2. Cancer letters 18 25128652
2010 Synthesis of the glycosaminoglycan-protein linkage tetraosyl peptide moieties of betaglycan, which serve as a hexosamine acceptor for enzymatic glycosyl transfer. Carbohydrate research 18 20813352
2009 Reducing betaglycan expression by RNA interference (RNAi) attenuates inhibin bioactivity in LbetaT2 gonadotropes. Molecular and cellular endocrinology 17 19524135