◀ Back to EPHB2
EPHB2 — SMN1
Text-mined interactions from Literome
Wang et al., Am J Physiol Heart Circ Physiol 2003
(MAP Kinase Signaling System) :
ERK was not activated by force, but p38 phosphorylation was
required for force induced inhibition of
SMA expression
Hu et al., Lung 2006
:
The induction of
alpha-SMA by TGF-beta1 was
suppressed by p38 kinase inhibitor ( SB203580 ) and
Erk inhibitor ( PD98059 ) ... Based on these findings, we conclude that p38 kinase,
Erk , and AP-1 are
responsible for the
alpha-SMA expression induced by TGF-beta1 in human fetal lung fibroblasts ...
Erk is
involved in inducing
alpha-SMA expression via AP-1 activation
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
Bondi et al., J Am Soc Nephrol 2010
:
In addition, TGF-beta1 stimulated phosphorylation of extracellular signal regulated kinase ( ERK1/2 ), and this was inhibited by blocking TGF-beta1 receptor 1, Smad3, or the Nox oxidases ;
ERK1/2 activation
increased alpha-SMA and Fn-ED-A
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