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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