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MSTN — SMAD3

Text-mined interactions from Literome

Langley et al., J Biol Chem 2002 : Myostatin signaling specifically induced Smad 3 phosphorylation and increased Smad 3.MyoD association, suggesting that Smad 3 may mediate the myostatin signal by interfering with MyoD activity and expression
Allen et al., Am J Physiol Cell Physiol 2007 : Here we examined the role of FoxO1 and SMAD transcription factors in regulating myostatin gene expression and myoblast differentiation in C ( 2 ) C ( 12 ) myotubes in vitro
Guo et al., J Biol Chem 2008 : Myostatin induced phosphorylation of Smad3 in hMSCs ; knockdown of Smad3 by RNAi or inhibition of its upstream kinase by an Alk5 inhibitor blocked the inhibitory effect of myostatin on adipogenesis in hMSCs, implying an important role of Smad3 activation in this event
Costelli et al., Eur J Clin Invest 2008 (Cachexia...) : In day 4 tumour hosts muscle myostatin levels were comparable to controls, yet follistatin was reduced, and SMAD DNA binding activity was enhanced
Yuzawa et al., Bone 2009 : Knockdown of Arkadia increased the Myostatin induced phosphorylation of Smad2/3 in C2C12 cells
Miyake et al., Biochem Biophys Res Commun 2010 : Overexpression of TIEG1 prevented the transcriptional activation of Smad by myostatin and TGF-beta in both proliferating or differentiating C2C12 cells, but the expression of Smad2 and Smad7 mRNAs was not affected
Bo Li et al., J Cell Sci 2012 (Fibrosis...) : Here, we demonstrate that myostatin also regulates the proliferation of dystrophic muscle fibroblasts, and increases resistance of fibroblasts to apoptosis through Smad and MAPK signaling
Watts et al., Am J Physiol Cell Physiol 2013 : Free myostatin induces the phosphorylation of the Smad family of transcription factors, which, in turn, regulates gene expression, via the canonical TGF-ß signaling pathway