IndraLab

Statements


TGFB1 activates SMAD4. 6 / 6
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"We have shown previously that the transforming growth factor-beta (TGFbeta)-regulated Sma-Mad (Smad) protein 3 and Smad4 proteins transactivate the apolipoprotein C-III promoter in hepatic cells"

"Furthermore, expression of dominant negative Smad3 or Smad4 in cells decreased or abolished the stimulation of beta(5) promoter activity by TGF-beta. Smad4 mutant also inhibited the up-regulation of surface beta(5) level by TGF-beta. Thus, TGF-beta increases expression of the integrin beta(5) gene by mechanisms involving Sp1/Sp3 and Smad transcription factors."

"The expression of JunD colocalised with pSmad 3 in fibrotic skin and silencing of Smad 3 or Smad 4 by siRNA prevented the induction of JunD by TGFbeta......The expression of JunD was analysed by real-time PCR, immunofluorescence, western blotting and immunohistochemistry. "

"Previously we have reported that the intracellular effectors of TGF-beta, Smad3 and Smad4, functionally cooperate with Sp1 to activate the human p21 promoter in hepatoma HepG2 cells."

"Second, silencing of SMAD protein levels using short interfering RNAs revealed that TGFbeta-induced activation of the endogenous gadd45beta gene required SMAD3 and SMAD4 but not SMAD2"

"activin A, TGF-beta1, and bone morphogenic protein 4 (BMP-4) bind to their respective receptor, a regulatory Smad is phosphorylated and becomes associated with Smad4, the common Smad, and the resulting complex translocates to the nucleus to regulate transcription"