"We have demonstrated that PR-619 suppressed UUO induced upregulation of Smad4 but not TGF-beta receptors, Smad2, or Smad3."
"Furthermore, KLF10 overexpression enhanced the TGFbeta induced Smad2 phosphorylation and increased the transcription of Smad2, but not Smad3 or Smad4 [XREF_BIBR]."
"For instance, phosphorylated Smad-2 can activate the Wnt/β-catenin signaling pathway independently of Smad-4 through p300 [ xref ]."
"the receptor-regulated Smad, such as Smad2, forms a heterocomplex with the co-mediator Smad, Smad4"
"Overexpression of Smad2 increases endogenous Smad4 and TGF-beta 1 expression while heterozygous loss of Smad2 reduces their expression levels, suggesting a concerted action of Smad2 and -4 in regulating TGF-beta signaling during skin development."
"Through analyzing the publicly available algorithms, including TargetScan, miRWalk, and miRanda, we found that several components of TGF-beta signaling, including SMAD2, SMAD4, and TGFBRI, may be potential targets of miR-582-3p, and SMAD2, SMAD4, TGFBRI, and TGFBRII for miR-582-5p (XREF_SUPPLEMENTARY A-S4C)."
"This causes phosphorylation of SMAD2 and SMAD3, two transcription factors that then bind to and activate SMAD4."
"That overexpression of Smad3 and Smad4, but not Smad2, decreased Galectin-3 promoter activity, while Smad3 silencing inhibited the promoter activity clearly indicated that the Galecin-3 promoter activity was responsive to Smad3."
"We have previously demonstrated that phosphorylated Smad2 can activate the Wnt/β-catenin signaling pathway independently of Smad4 [ xref ]."