IndraLab

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TGFBR2 activates SMAD3. 10 / 10
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"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]."
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"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."
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"Tbeta RII activates Tbeta RI, which, in turn, propagates the TGF-beta signal by phosphorylating the Smads, in particular Smad2 and Smad3 (Massague & Chen, 2000)."
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"Taken together, these results suggest that Abeta42 induced increases in neuronal alpha1 (VI) expression involve TbetaRII dependent activation of Smad3."
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"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 ."
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"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."
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"When released from LAP (latency-associated peptide) and LTBP (latent TGF-β-binding protein), active TGF-β1 binds with its type II receptor that activates type I receptor and downstream effectors, Smad2 and Smad3, to regulate genes associated with renal fibrosis xref ."
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"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."
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"The binding of TGF-β to its receptors TGFR1 and TGFR2 activates Smad2 and Smad3 through direct phosphorylation."
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"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."
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Kinase-active TGFBR2 activates SMAD3. 2 / 2
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"\"Smad proteins mediate signaling by transforming growth factor-beta (TGF-beta) 1 superfamily members (1-3). Upon binding of TGF-beta to cell surface complexes of type I and type II receptor serine/threonine kinases, the type II receptor phosphorylates the type I receptor, which further phosphorylates the receptor-regulated (R-) Smads, Smad2 and Smad3 (3). Phosphorylated R-Smads oligomerize with the common mediator (Co) Smad4 and accumulate in the nucleus where they regulate gene expression.\""
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"\"Smad proteins mediate signaling by transforming growth factor-beta (TGF-beta) 1 superfamily members (1-3). Upon binding of TGF-beta to cell surface complexes of type I and type II receptor serine/threonine kinases, the type II receptor phosphorylates the type I receptor, which further phosphorylates the receptor-regulated (R-) Smads, Smad2 and Smad3 (3). Phosphorylated R-Smads oligomerize with the common mediator (Co) Smad4 and accumulate in the nucleus where they regulate gene expression.\""
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TGFBR2 bound to TGFBR1 activates SMAD3. 2 / 2
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"The TbetaRII and ALK-5 complex activates Smad2 and Smad3, whereas the TbetaRII and ALK-1 complex activates Smad1, Smad5 and Smad8 [51]."
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"Of the five R-Smads in mammals, the TGFBR2 and ALK5 complex activates SMAD2 and SMAD3, whereas the TGFBR2 and ALK1 complex activates SMAD1, SMAD5 and SMAD8 XREF_BIBR."
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TGFBR2 bound to ALK5 receptor activates SMAD3. 1 / 1
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"TGF-beta signalling is mediated by the TbetaRII and ALK5 receptor complex activating the Smad2 and Smad3 pathway."
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Catalytically active TGFBR2 activates SMAD3. 1 / 1
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"Furthermore, acute and long-term pretreatment of ECs with thrombin or PAR1 peptide agonist suppressed the TGF-beta-induced serine phosphorylation of Smad2, a critical mediator of TGF-beta signaling. Moreover, activation of PAR1 led to a profound and spread cytosolic clustering formation of Smad2/3 and markedly prevented Smad2/3 nuclear translocation evoked by TGF-beta1."
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