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1 ta) receptor (TbetaRIII, also referred to as betaglycan).
2 ociation with the transmembrane proteoglycan betaglycan.
3 pe III TGF-beta receptor Tgfbr3, also called betaglycan.
4 domain as the only inhibin-binding region in betaglycan.
5 tors, and this competition is facilitated by betaglycan.
6 hich does not bind inhibin in the absence of betaglycan.
7 on of the glycosaminoglycan modifications of betaglycan.
8 pithelial LLC-PK1 cells that lack endogenous betaglycan.
9 es binding in cells co-expressing ActRII and betaglycan.
10 he type III TGF-beta receptor (TbetaRIII, or betaglycan), a ubiquitously expressed TGF-beta corecepto
11 ral human and animal diseases, although both betaglycan actions and the ligands involved in these dis
13 viously that ectopic expression of a soluble betaglycan, also known as transforming growth factor (TG
14 oglin has homology to the type III receptor, betaglycan, although its exact role in TGF-beta signalin
16 es identify a novel, dual role for TbetaRIII/betaglycan and define a key requirement for the balance
25 Inhibin, in concert with its co-receptor, betaglycan, can compete with activin for binding to type
26 ngs demonstrate that inhibin, acting through betaglycan, can function as an antagonist of BMP respons
27 we show that the type III TGF-beta receptor, betaglycan, can function as an inhibin co-receptor with
31 for the first time, epigenetic regulation of betaglycan expression in ovarian cancer, and a novel rol
36 hat type III TGF-beta receptor (TbetaRIII or betaglycan) expression is decreased or lost in the major
37 a domain spanning amino acids 591-700 of the betaglycan extracellular domain as the only inhibin-bind
39 luble TGF-beta type III receptor (TbetaRIII; betaglycan)-Fc reconstituted a soluble high affinity inh
41 s of betaglycan expression, or abrogation of betaglycan function, is implicated in several human and
42 will allow the clarification of the role of betaglycan in disease states such as renal cell carcinom
47 sion in ovarian cancer, and a novel role for betaglycan in regulating ovarian cancer motility and inv
49 s, suggesting a broader role for inhibin and betaglycan in restricting and refining a wide spectrum o
52 genetic and biochemical evidence showed that betaglycan is not a substrate of the shedding system.
53 wth factor beta type III receptor (TbetaRIII/betaglycan) is a transmembrane proteoglycan co-receptor
54 The TGF-beta type III receptor (TbetaRIII or betaglycan) is an abundant cell surface proteoglycan tha
55 GF-beta) receptor (TbetaRIII), also known as betaglycan, is the most abundantly expressed TGF-beta re
56 lted in significant synergistic induction of betaglycan message levels and increased betaglycan prote
57 an (GAG) chains than in L6 cells, and a GAG- betaglycan mutant does not inhibit TGF-beta signaling or
59 the type III TGF-beta receptor (TbetaRIII or betaglycan), occurs in a broad spectrum of human cancers
61 LC-PK1 cells, unlike L6 cells, expression of betaglycan prevents association between the type I and t
62 n of betaglycan message levels and increased betaglycan protein expression, indicating that epigeneti
64 he type III TGF-beta receptor (TbetaRIII, or betaglycan) serves as a novel suppressor of cancer progr
66 F-beta-mediated inhibition of proliferation, betaglycan significantly inhibits ovarian cancer cell mo
67 se we chose the TGF-beta accessory receptor, betaglycan, since genetic and biochemical evidence showe
72 rodimer, in conjunction with the co-receptor betaglycan, to block activin receptor-ligand binding, co
74 TGF-beta2 appears to require the co-receptor betaglycan (type III receptor, TbetaRIII) for high affin
78 cids adjacent to the transmembrane region of betaglycan with the corresponding regions of TGF-alpha o
80 he 2.0-A resolution crystal structure of the betaglycan ZP-C region in combination with a downstream
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