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1 gical inhibition of activin-like kinase-5, a type I TGF-beta receptor.
2 t UCH37 can deubiquitinate and stabilize the type I TGF-beta receptor.
3 reby preventing it from interacting with the type I TGF-beta receptor.
4 ich is enhanced after phosphorylation by the type I TGF-beta receptor.
5 ner since it can bind to ALK-1 as well as to type I TGF-beta receptor.
6 tes TGF-beta signaling through ALK-1 and the type I TGF-beta receptor.
7 ll clone expresses one mutant allele for the type I TGF-beta receptor.
8 A, associates with the cytoplasmic domain of type I TGF-beta receptors.
9 show in the same cells that, conversely, the type I TGF-beta receptor activin receptor-like kinase 5
10 activin binding to ALK4 are conserved on the type I TGF-beta receptor ALK5, suggesting the correspond
11 I-K277R is expressed, can associate with the type I TGF-beta receptor, and block both Smad-dependent
12 imerization of the cytoplasmic domain of the type I TGF-beta receptor are required for intracellular
14 r was found to form heterocomplexes with the type I TGF-beta receptor by immunoprecipitation with ant
15 fected with Smad3 or a constitutively active type I TGF-beta receptor, exhibit increased ubiquitinati
17 ent with TGF-beta-neutralizing antibodies, a type I TGF-beta receptor kinase inhibitor, or activin-ne
18 s abrogated by pharmacological inhibition of type I TGF-beta receptor kinase, combined inhibition of
19 LR axis determination, nor is it known which type I TGF beta receptor(s) are involved in mediating le
20 ctory learning, and that the activity of the type I TGF-beta receptor SMA-6 in the hypodermis is need
23 ich associates with both SmRK1 and the human type I TGF beta receptor (T beta RI); overexpression of
24 e II TGF-beta receptor (T beta RII), and the type I TGF-beta receptor (T beta RI) to regulate diverse
25 fective mutant cells (DR26 cells) but not in type I TGF-beta receptor (TbetaR-I)-defective mutant cel
26 filing proteins that differentially bound to type I TGF-beta receptor (TbetaRI) in nontransformed, HE
27 echanistically, fibulin-3 interacts with the type I TGF-beta receptor (TbetaRI) to block TGF-beta ind
28 the lateral mobility and endocytosis of the type I TGF-beta receptor (TbetaRI) with TGF-beta phospho
29 Although Smad7 did not associate with the type I TGF-beta receptor (TbetaRI), SB-431542, an inhibi
34 nce that a common hypomorphic variant of the type I TGF-beta receptor, TGFBR1*6A, may account for app
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