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MAPK3 — SMN1
Text-mined interactions from Literome
McCarroll et al., Pancreas 2003
(MAP Kinase Signaling System) :
However, inhibition of
ERK 1/2 and JNK
had no effect on ethanoland acetaldehyde induced
alpha-SMA expression in PSCs
Huang et al., Zhonghua Yi Xue Za Zhi 2005
:
Inhibition of
Erk-1/2 activation by Mek kinase inhibitor PD98059 suppressed CTGF mediated myofibroblasts proliferation and significantly
down-regulated expression of
alpha-SMA protein in cells pretreated by TGF-beta(1) ( P < 0.05 )
Shen et al., Biochem Biophys Res Commun 2006
:
Inhibiting
p38MAPK with SB202190 or JNK with SP600125 also
reduced angiotensin II-induced
alpha-SMA expression
Giannopoulou et al., American journal of physiology. Renal physiology 2006
(Fibrosis...) :
Constitutive activation of
Erk-1/2 by ectopic expression of activated Mek1 mimicked IFN-gamma and
suppressed TGF-beta(1) mediated
alpha-SMA expression
Vepachedu et al., J Immunol 2007
(MAP Kinase Signaling System...) :
Blocking p38
MAPK resulted in reduced
alpha-SMA expression by Unc119 suggesting that the p38 pathway regulates Unc119 induced myofibroblast differentiation
Ding et al., J Biol Chem 2008
(Disease Models, Animal...) :
Although both ERK and p38
MAPK activation is
required for maximal TGF-beta1 induced
alpha-SMA expression, ERK is the major signaling intermediate in cells that express FAK
Pappas et al., Eur J Vasc Endovasc Surg 2009
(Chronic Disease...) :
alpha-SMA protein expression in LC fibroblasts
increased with
MAPK inhibition with/without TGF-beta(1) stimulation, and correlated with the degree of gel contraction
Ishiguro et al., Wound Repair Regen 2009
:
Along with the inhibition of alpha-SMA expression by bFGF, the RMF and RMFL cells also showed different activated expression of extracellular signal regulated kinase 1/2, suggesting the
involvement of
extracellular signal regulated kinase 1/2 activation in the down-regulation of
alpha-SMA expression in myofibroblasts
Liu et al., Nan Fang Yi Ke Da Xue Xue Bao 2011
(Scleroderma, Systemic) :
In the presence of TGF-ß ( 1 ), blocking of Smads,
ERK/MAPK , and p38MAPK pathways, but not JNK/MAPK pathway,
caused an obvious decrease in
a-SMA levels in the fibroblasts in both groups