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1 rane and cytoplasmic domain of the type I or type II TGF beta receptor.
2 anced by ALK-1 and to a lesser extent by the type II TGF-beta receptor.
3 we characterized the kinase activity of the type II TGF-beta receptor.
4 ory response in the absence of the type I or type II TGF-beta receptor.
5 le Ect SMCs elaborate only an unglycosylated type II TGF-beta receptor.
6 rane and cytoplasmic domain of the type I or type II TGF-beta receptor.
7 ar signals are referred to as the type I and type II TGF beta receptors.
8 -beta receptor but expressing the type I and type II TGF-beta receptors.
10 ein, and increased mRNAs encoding TGF-beta1, type II TGF-beta receptor, alpha1(IV) collagen, and fibr
11 n requires cross-talk between the type I and type II TGF beta receptors and that TGF beta receptor he
12 n/spreading, and mediated by upregulation of type II TGF-beta receptor and connective tissue growth f
13 lls do not express either alpha5 integrin or type II TGF-beta receptor and hence are unable to genera
14 n despite the expression of normal levels of type II TGF-beta receptors and normal levels of phosphor
15 STRAP, that associates with both type I and type II TGF-beta receptors and that is involved in TGF-b
16 ecreted Klotho protein directly binds to the type-II TGF-beta receptor and inhibits TGF-beta1 binding
17 or plasminogen activator inhibitor 1 and the type II TGF-beta receptor, and they synergize with TGF-b
18 a functional EN protein tyrosine kinase, and type II TGF-beta receptor appears to be a direct target
19 within 24 hours post-wounding) of type I and type II TGF-beta receptors as well as unexpectedly high
20 assage MCF-7 cells, which exhibit detectable type II TGF-beta receptors at the cell surface and exqui
22 oreover, suramin decreased expression of the type II TGF-beta receptor, blocked phosphorylation of th
25 the second suggests that distinct type I or type II TGF-beta receptor combinations mediate aspects o
26 further show that reduced expression of the type II TGF-beta receptor correlates with loss of lumina
27 e response elicited by defined type I and/or type II TGF-beta receptor cytoplasmic domain homomers or
28 lls and to a lesser extent of the type I and type II TGF-beta receptor-defective mutants, although hi
29 ic mice that overexpress a dominant negative-type II TGF-beta receptor (delta beta RII) in the epider
30 tion to introduce a dominant-negative mutant type II TGF-beta receptor (DNR) into the premalignant ra
31 signaling, by stably expressing a truncated type II TGF-beta receptor, enhanced differentiation and
33 ressing a TGF-beta antagonist of the soluble type II TGF-beta receptor:Fc fusion protein class, under
34 ALK-1/ligand interaction is mediated by the type II TGF-beta receptor for TGF-beta and most likely t
35 ce by expressing a cytoplasmically truncated type II TGF-beta receptor from the osteocalcin promoter.
36 ression in the adult and show that the DAF-4 type II TGF-beta receptor functions cell-autonomously to
37 al studies observed that the promoter of the type II TGF-beta receptor gene (TbetaR-II) is strongly s
38 studies have shown that the promoter of the type II TGF-beta receptor gene (TbetaR-II) is strongly s
39 e protein and mRNA transcripts of type I and type II TGF-beta receptor genes were detectable in psori
40 e ryanodine receptor, aspartokinase, and the type II TGF-beta receptor; however, none of these are co
41 ammary gland and conditional deletion of the type II TGF-beta receptor in mammary epithelium, an incr
45 nding of their cognate ligands to type I and type II TGF-beta receptors, indicating that Cripto-1 and
46 tion, we have introduced a dominant negative type II TGF-beta receptor into a series of genetically r
49 coexpression of apically targeted type I and type II TGF-beta receptors mediated Smad3 signaling from
50 oliferation, and increased the expression of type II TGF-beta receptor mRNA and cell surface protein.
51 at the cytoplasmic domains of the type I and type II TGF-beta receptors physically and functionally i
52 domain, in complex with the B-site of mouse type II TGF-beta receptor promoter DNA (mTbetaR-II(DNA))
54 dle T-induced mammary carcinomas lacking the type II TGF-beta receptor (PyMT(mgko)) are highly metast
55 or ERK2 activation in ZR-75 BCCs lacking the type-II TGF-beta receptors (R(II)), or in ZR-75 BCCs sta
56 search for proteins that associate with the type II TGF beta receptor (RII), we isolated a protein w
59 a polyclonal antibody specific for the chick type II TGF-beta receptor subunit, we demonstrate that M
60 astases in mice bearing tumors that lack the type II TGF-beta receptor, suggesting that the increase
62 combinase (WAP-Cre), we have now ablated the type II TGF-beta receptor (T beta RII) expression specif
63 ype III TGF-beta receptor (T beta RIII), the type II TGF-beta receptor (T beta RII), and the type I T
65 genous beta-glucuronidase in Mv1Lu cells and type II TGF-beta receptor (TbetaR-II)-defective mutant c
67 with S2 increased the amounts of type I and type II TGF-beta receptors (TbetaRI and TbetaRII), where
68 nduced complex formation of TbetaRI with the type II TGF-beta receptor (TbetaRII) and subsequent down
69 ctions between the cytoplasmic domain of the type II TGF-beta receptor (TbetaRII) and the FN receptor
71 ated with a 95% decrease in the level of the type II TGF-beta receptor (TbetaRII) protein, a 40-fold
72 s dependent on the heterodimerization of the type II TGF-beta receptor (TbetaRII) with the type I TGF
73 nd activation of the serine/threonine kinase type II TGF-beta receptor (TbetaRII), which in turn prom
74 er, such phosphorylation was mediated by the type II TGF-beta receptor (TbetaRII), which is itself a
78 induced the internalization of endoglin and type-II TGF-beta receptor (TbetaRII) but not type-I rece
79 t gene-based expression of dominant-negative type II TGF-beta receptor (TGF-beta-RII-DN) in the poste
80 ta receptor complex consisting of type I and type II TGF-beta receptors (TGFBR1 and TGFBR2), regulate
81 esulting in a 1,4-dihydropyridine inducer of type II TGF-beta receptor (TGFBR2) degradation-1 (ITD-1)
82 F-beta, is deleted or mutated in 55% and the type II TGF-beta receptor (Tgfbr2) gene is altered in a
83 rigenesis, and metastasis, the gene encoding type II TGF-beta receptor, Tgfbr2, was conditionally del
84 GF-beta signaling by directly binding to the type II TGF-beta receptor, thereby preventing it from in
86 ssing a dominant-negative mutant form of the type II TGF-beta receptor, under the control of the mous
87 Using cre-lox technology, expression of the type II TGF-beta receptor was selectively knocked out in
88 on 2 of the TbetaRII gene, which encodes the type II TGF-beta receptor, was deleted via a mesodermal-
89 prevents association between the type I and type II TGF-beta receptors, which is required for signal
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