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MSTN — SMAD2
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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
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
Ciarmela et al., Endocrinology 2009
:
Functional assays showed that
myostatin induced phosphorylation of
Smad-2 and reduced proliferation of PHM1 number in a time and dose dependent manner
Yuzawa et al., Bone 2009
:
Knockdown of Arkadia increased the
Myostatin induced phosphorylation of
Smad2/3 in C2C12 cells
Watt et al., Muscle Nerve 2010
(Hypertrophy) :
SB431542 treatment reduced
myostatin induced C-terminal
Smad2 phosphorylation and resulted in the formation of enlarged myotubes
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