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SMAD3 — SMN1

Text-mined interactions from Literome

Sumiyoshi et al., J Invest Dermatol 2004 (Disease Models, Animal...) : Consistent with the in vivo findings, overexpression of Smad3 induced alpha-SMA , VEGF, and TGF-beta1 expression and augmented chemotactic response in cultured dermal fibroblasts
Subramanian et al., Mol Biol Cell 2004 : A novel Sp1 : Pur : SPUR complex was dissociated when SMA enhancer activity was increased by TGFbeta1 or Smad protein overexpression
Phanish et al., Biochem J 2006 : Increases in alpha-SMA expression were dependent on both Smad2 and Smad3 and were abolished by combined knockdown of both Smad2 and Smad3
Kobayashi et al., Biochem Biophys Res Commun 2006 : Using small interference RNA ( siRNA ), the role of Smad2 and Smad3 in TGF-beta stimulation of human lung fibroblast contraction of collagenous matrix and induction of alpha-SMA and the role of alpha-SMA in contraction were assessed ... Thus, Smad3 mediates TGF-beta1 induced contraction and alpha-SMA induction in human lung fibroblasts
Aoki et al., Am J Physiol Cell Physiol 2007 : Moreover, dominant negative Smad2/3 expression attenuated the expression of COX-2 and alpha-SMA enhanced by IL-1beta and IL-6
Hu et al., Am J Respir Cell Mol Biol 2007 : Since TGF-beta- induced alpha-SMA expression is Smad3 dependent , potential interaction between GKLF and Smad3 was examined as a basis for this additional inhibitory mechanism
Gu et al., Acta Pharmacol Sin 2007 : We found that the overexpression of Smad3 , not Smad2 markedly increased ( TGF)-beta(1 ) -induced alpha-SMA promoter activity and alpha-SMA protein expression in vitro, whereas the overexpression of dominant negative mutant Smad3 and Smad7 repressed ( TGF)-beta(1 ) -induced alpha-SMA gene expression
Masszi et al., J Cell Biol 2010 (Fibrosis) : Surprisingly, Smad3 inhibits MRTF-driven activation of the SMA promoter, and Smad3 silencing renders injury sufficient to induce SMA expression
Amara et al., Thorax 2010 (Idiopathic Pulmonary Fibrosis) : It was found that ( 1 ) NOX4 mRNA and protein expression was upregulated in pulmonary fibroblasts from patients with IPF and correlated with mRNA expression of alpha-SMA and procollagen I ( alpha1 ) mRNA ; ( 2 ) TGFbeta1 upregulated NOX4, alpha-SMA and procollagen I ( alpha1 ) expression in control and IPF fibroblasts ; ( 3 ) the change in alpha-SMA and procollagen I ( alpha1 ) expression in response to TGFbeta1 was inhibited by antioxidants and by a NOX4 small interfering RNA ( siRNA ) ; ( 4 ) NOX4 modulated alpha-SMA and procollagen I ( alpha1 ) expression by controlling activation of Smad2/3 ; and ( 5 ) NOX4 modulated PDGF induced fibroblast migration
Guo et al., Am J Physiol Cell Physiol 2011 : Coexpression of RGC-32 and Smad3 , but not Smad2, induces a higher mesenchymal marker a-smooth muscle actin ( a-SMA ) protein expression as compared with RGC-32 or Smad3 alone, while knockdown of Smad3 using short hairpin interfering RNA blocks RGC-32 induced a-SMA expression
Li et al., J Biol Chem 2011 (Disease Models, Animal...) : Functionally, RGC-32 is crucial for Smad3 mediated a-SMA promoter activity