IndraLab
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"TGF-beta exerts its pro fibrotic effects through transcription factor signaling Smad3, and selective inhibition of Smad3 phosphorylation and inhibition of Smad3 interaction with Smad4 has been shown to reduce fibroblast activation to the myofibroblast phenotype and also reduce ECM synthetic activity of the cells."
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"Furthermore, both SMAD2 and SMAD3 are activated by phosphorylation, and our results support that patients whose TAFs exhibit a low (<1) pSMAD3/pSMAD2 ratio may be refractory to nintedanib and possibly to other antifibrotic drugs, whereas those with high (>1) pSMAD3/pSMAD2 ratio may elicit positive responses (where pSMAD2 and pSMAD3 refers to phosphorylated SMAD2 and SMAD3, respectively) (Figure 3D)."
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"Notably, CerS4 knockdown had no significant effect on endogenous Smad7 protein abundance (XREF_FIG, bottom) or canonical TGF-beta signaling compared to Scr shRNA transfected A549 controls, measured by Smad3 dependent luciferase reporter assay (XREF_FIG), and phosphorylation of Smad3 using Western blotting with and without TGF-beta exposure (XREF_FIG)."
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"The second scenario is that HEF1 tethers Smad3 in a cytoplasmic complex and the type I receptor activation leads to phosphorylation of Smad3 and the subsequent conformational changes that can enhance its interaction with APC10, which recruits the APC ligase and assists CDH1 to bind the substrate HEF1."
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"We detected the change of Smad3 in anti-CD3/CD28 stimulated splenic CD4+ T cells by western blot and indicated significant upregulation of both total Smad3 and phosphorylated Smad3 in oral atorvastatin treatment group ( ∗ P < 0.05, as in xref ); more interestingly, the knockout of GARP by GARP-siRNA inhibited the upregulation of Smad3 and p-Smad3 induced by atorvastatin ( ∗∗ P < 0.05, as in xref )."
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"In normal chondrocytes, mechanotransduction signals induced the translocation of the nuclear factor of activated T-cells 3 (NFAT3) to the nucleus and subsequently activated the expression of miR-140, whereas in OA chondrocytes, overexpression of transforming growth factor-β (TGF-β) resulted in the phosphorylation of mothers against decapentaplegic homolog 3 (SMAD3) that directly inhibited miR-140 [33]."
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"After PGRN knockdown by siRNA, the expression of PGRN, collagen I (Col I), small mothers against decapentaplegic homolog 3 (Smad3), phosphorylated Smad3 (P-Smad3), transforming growth factor (TGF)-beta1 and TGF-beta receptor I (TbetaRI) were detected by real-time reverse transcription polymerase chain reaction (RT-qPCR) or Western blot."