"Increased expression levels of TGF-beta receptor II (TGFBR2) in MSCs from SSc patients under basal conditions and enhanced SMAD3 activation followed by increased collagen mRNA synthesis was recently independently reported upon short-term TGF-beta1 stimulation (up to 24 h) [XREF_BIBR]."
"In conclusion, in our model (XREF_FIG), we propose that expression of alpha v beta 6 integrin by associating with TbetaRII promotes Smad3 mediated downstream signaling pathway and consequent upregulation of MMP2 and MMP2 dependent cell migration in response to TGFbeta1."
"Taken together, these results suggest that Abeta42 induced increases in neuronal alpha1 (VI) expression involve TbetaRII dependent activation of Smad3."
"Of the five R-Smads in mammals, the TGFBR2–ALK5 complex activates SMAD2 and SMAD3, whereas the TGFBR2–ALK1 complex activates SMAD1, SMAD5 and SMAD8 xref ."
"Results indicated that knockdown of TbetaRII, confirmed by Western blotting analysis and RT-PCR (XREF_FIG), reduced both basal and TGF-beta1-induced P-Smad2 and P-Smad3 (XREF_FIG), as well as Smad responsive promoter activity as reported by luciferase activity (XREF_FIG), suggesting that autocrine TGF-beta signaling is also abrogated by TbetaRII knockdown."
"20 During TGF-beta pathway mediated hypertrophic scar formation, there is an up-regulation of SMAD-2 and SMAD-3, as well as increased expression of TGF-beta1, TbetaRI and TbetaRII, which lead to positive feedback loop."
"The EOB phenotype was observed in mice lacking the type I BMP receptor genes, Acvr1 and Bmpr1a, the R-Smad genes, Smad 1 and Smad5, and the Co-Smad gene, Smad 4, but not in mice lacking the type II TGFbeta receptor gene Tgfbr2 and the activin and TGFbeta activated R-Smad genes, Smad2 and Smad3."