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1 ta) receptor (TbetaRIII, also referred to as betaglycan).
2 pe III TGF-beta receptor Tgfbr3, also called betaglycan.
3 ociation with the transmembrane proteoglycan 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 fferentially induced genes in MSC, including betaglycan, a co-receptor for TGFbeta.
12 rked induction of canonical Wnt signaling in betaglycan ablated MSCs, and the addition of recombinant
13 induce the expression of osteogenic genes in betaglycan-ablated MSCs.
14 ral human and animal diseases, although both betaglycan actions and the ligands involved in these dis
15                                              Betaglycan also enables inhibin to bind to and compete w
16 viously that ectopic expression of a soluble betaglycan, also known as transforming growth factor (TG
17 oglin has homology to the type III receptor, betaglycan, although its exact role in TGF-beta signalin
18  both recombinant and endogenously expressed betaglycan and ActRII.
19 es identify a novel, dual role for TbetaRIII/betaglycan and define a key requirement for the balance
20          Nonpolymerizing ZP proteins such as betaglycan and endoglin do not contain this cleavage sit
21                   Other ZP proteins (namely, betaglycan and endoglin) do not polymerize but serve as
22                                    Recently, betaglycan and inhibin binding protein (InhBP/p120, also
23 ntrast, female mice lacking both TGFBR3L and betaglycan are infertile.
24                                  We identify Betaglycan as a unique marker of self-renewing MuSCs tha
25                                              Betaglycan (BG) is a membrane-bound co-receptor of the T
26                                              Betaglycan (BG) is a transmembrane co-receptor of the tr
27                                              Betaglycan binds inhibin with high affinity and enhances
28         The type III receptor, also known as betaglycan, binds to the type II receptor and is thought
29 an-2 specifically co-immunoprecipitated with betaglycan but not with TbetaRI or TbetaRII.
30                                              Betaglycan can confer inhibin responsiveness on cells th
31                       Our data indicate that betaglycan can function as a potent inhibitor of TGF-bet
32    Inhibin, in concert with its co-receptor, betaglycan, can compete with activin for binding to type
33 ngs demonstrate that inhibin, acting through betaglycan, can function as an antagonist of BMP respons
34 we show that the type III TGF-beta receptor, betaglycan, can function as an inhibin co-receptor with
35                                     Finally, betaglycan confers inhibin sensitivity to cell lines tha
36 istically, gene expression analysis revealed betaglycan controls the expression of a large repertoire
37 ssion of the metastasis suppressor TbetaRIII/betaglycan decreases invasiveness.
38               Inhibiting either signaling or betaglycan expression attenuated differentiation.
39 for the first time, epigenetic regulation of betaglycan expression in ovarian cancer, and a novel rol
40                           Although restoring betaglycan expression in Ovca429 ovarian cancer cells is
41                           Here, we show that betaglycan expression is frequently decreased or lost in
42 tic silencing may play a role in the loss of betaglycan expression observed in ovarian cancer.
43                                      Loss of betaglycan expression, or abrogation of betaglycan funct
44 hat type III TGF-beta receptor (TbetaRIII or betaglycan) expression is decreased or lost in the major
45 a domain spanning amino acids 591-700 of the betaglycan extracellular domain as the only inhibin-bind
46 orming growth factor-beta type III receptor, betaglycan, fails to interact with zyxin.
47 luble TGF-beta type III receptor (TbetaRIII; betaglycan)-Fc reconstituted a soluble high affinity inh
48                         We now show that the betaglycan form of TbetaRIII is highly modified followin
49 s of betaglycan expression, or abrogation of betaglycan function, is implicated in several human and
50                                              Betaglycan has not been studied in the context of bone m
51  will allow the clarification of the role of betaglycan in disease states such as renal cell carcinom
52             In comparison, the expression of betaglycan in L6 myoblasts enhances TGF-beta signaling,
53                               The effects of betaglycan in LLC-PK1 cells are not mediated by ligand s
54                                              Betaglycan in LLC-PK1 cells exhibits higher molecular we
55        We demonstrate that the expression of betaglycan in LLC-PK1 cells results in inhibition of TGF
56                  Here we report that loss of betaglycan in MSC is sufficient to augment TGFbeta signa
57 sion in ovarian cancer, and a novel role for betaglycan in regulating ovarian cancer motility and inv
58             We have examined the function of betaglycan in renal epithelial LLC-PK1 cells that lack e
59 s, suggesting a broader role for inhibin and betaglycan in restricting and refining a wide spectrum o
60                                              Betaglycan increases the affinity of inhibins for the ac
61                                              Betaglycan is a co-receptor that mediates signaling by t
62 genetic and biochemical evidence showed that betaglycan is not a substrate of the shedding system.
63 wth factor beta type III receptor (TbetaRIII/betaglycan) is a transmembrane proteoglycan co-receptor
64 The TGF-beta type III receptor (TbetaRIII or betaglycan) is an abundant cell surface proteoglycan tha
65                  The TGFB type III receptor, betaglycan, is required for inhibin A suppression of FSH
66 GF-beta) receptor (TbetaRIII), also known as betaglycan, is the most abundantly expressed TGF-beta re
67  large repertoire of genes in MSCs, and that betaglycan loss provokes >60-fold increase in the expres
68                                              Betaglycan mediates the actions of both inhibins and is
69 lted in significant synergistic induction of betaglycan message levels and increased betaglycan prote
70 an (GAG) chains than in L6 cells, and a GAG- betaglycan mutant does not inhibit TGF-beta signaling or
71                                        These betaglycan mutants fail to mediate inhibin antagonism of
72 the type III TGF-beta receptor (TbetaRIII or betaglycan), occurs in a broad spectrum of human cancers
73                                              Betaglycan, or the type III TGF-beta receptor, is a core
74 LC-PK1 cells, unlike L6 cells, expression of betaglycan prevents association between the type I and t
75 n of betaglycan message levels and increased betaglycan protein expression, indicating that epigeneti
76 mbinant preparation of human and rat soluble betaglycan (sBG).
77 he type III TGF-beta receptor (TbetaRIII, or betaglycan) serves as a novel suppressor of cancer progr
78               A third cell surface receptor, betaglycan, serves as a co-receptor for TGF-beta in some
79 F-beta-mediated inhibition of proliferation, betaglycan significantly inhibits ovarian cancer cell mo
80 se we chose the TGF-beta accessory receptor, betaglycan, since genetic and biochemical evidence showe
81                                 Furthermore, betaglycan specifically enhances the antimigratory effec
82 ng regions of TGF-alpha or beta-APP rendered betaglycan susceptible to ectodomain shedding.
83 red to as the type I, type II, and type III (betaglycan) TGF-beta receptors.
84 I receptors in concert with the co-receptors betaglycan (TGFBR3) and TGFBR3L.
85                               The ability of betaglycan to facilitate inhibin antagonism of activin p
86 rodimer, in conjunction with the co-receptor betaglycan, to block activin receptor-ligand binding, co
87        Separating the co-receptor actions of betaglycan toward inhibin and TGFbeta will allow the cla
88 TGF-beta2 appears to require the co-receptor betaglycan (type III receptor, TbetaRIII) for high affin
89                                  Full-length betaglycan V614Y, and other mutations, retain TGFbeta bi
90 ssion of the HS proteoglycans syndecan 4 and betaglycan was reduced.
91                                     Further, betaglycan was revealed as necessary for prostate cancer
92 eceptors type I (ALK), type II (ACTRII), and betaglycan were analyzed in PAH and control lung tissues
93 l of type III TGF-beta receptor (TbetaRIII), betaglycan, whereas S2 resulted in a decrease.
94 s I and II receptors with t1/2 of 2 h and to betaglycan with t1/2 of 6 h.
95 cids adjacent to the transmembrane region of betaglycan with the corresponding regions of TGF-alpha o
96       Collectively, these findings suggest a betaglycan-Wnt5a circuit represents an attractive vulner
97              This binding site is within the betaglycan ZP domain, but inhibin binding is not integra
98 he 2.0-A resolution crystal structure of the betaglycan ZP-C region in combination with a downstream