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EPHB2 — SMAD2

Text-mined interactions from Literome

Leask et al., J Biol Chem 2003 : Now we show that protein kinase C and Ras/MEK/ERK are necessary for the TGF-beta induction of the CTGF promoter but not of a generic Smad-responsive promoter ( SBE-lux )
Dupont et al., Biol Reprod 2003 : Using specific inhibitors, we demonstrated that the activation of Smad-2 was partially blocked by the inhibition of PI3K but not by the inhibition of ERK1/2 or p38, suggesting a cross-talk between the Smad and PI3K/Akt pathways
Hayashida et al., FASEB J 2003 (MAP Kinase Signaling System) : This effect was not seen in the mouse mammary epithelial NMuMG cell line, indicating that ERK dependent activation of Smad2/3 occurs only in certain cell types ... These results indicate that ERK dependent R-Smad linker region phosphorylation enhances collagen I synthesis and imply positive cross talk between the ERK and Smad pathways in human mesangial cells
Xie et al., Am J Physiol Lung Cell Mol Physiol 2005 : Inhibition of ERK and c-jun NH ( 2 ) -terminal kinase ( JNK ), but not of p38 MAPK and PI3K, blocked the effect of TGF-beta 1 on CTGF mRNA and protein expression and on Smad2/3 phosphorylation
Rhyu et al., J Am Soc Nephrol 2005 (Fibrosis...) : Chemical inhibition of ERK but not p38 MAPK inhibited TGF-beta1 induced Smad 2 phosphorylation, and both MAPK inhibitors inhibited TGF-beta1- and H ( 2 ) O ( 2 ) -induced EMT
Nakagawa et al., J Am Soc Nephrol 2005 : Whereas blocking of ERK1/2 or p38 failed to inhibit TGF-beta1 induced Smad2 activation, inhibition of Smad2 by Smad7 overexpression inhibited the phosphorylation of ERK1/2 but not p38 in response to TGF-beta1 ... The ERK1/2 activation is dependent on Smad2 activation, whereas the p38 activation occurs independent of Smad2
Kfir et al., Mol Cell Biol 2005 : Pathway- and expression level dependent effects of oncogenic N-Ras : p27 ( Kip1 ) mislocalization by the Ral-GEF pathway and Erk mediated interference with Smad signaling
Wang et al., Circ Res 2006 (Arteriosclerosis...) : This was extracellular signal regulated kinase 1/2 ( ERK1/2 ) mitogen activated protein kinase ( MAPK ) dependent but transforming growth factor-beta ( TGF-beta ) independent because Ang II-induced Smad signaling was blocked by addition of ERK1/2 inhibitor and by dominant negative ( DN ) ERK1/2 but not by DN-TGF-beta receptor II (TbetaRII) or conditional deletion of TbetaRII
Wang et al., Mol Cell Biochem 2006 : Our results suggest that p38 affects the phosphorylation of Smad2 and Smad3 differentially during TGF-beta signaling in human dental pulp cells and ERK1/2 might be involved in the process
Hong et al., Translational research : the journal of laboratory and clinical medicine 2006 : TGF-beta activates extracellular signal regulated kinase ( ERK ) in mesangial cells, and ERK is involved in activation of Smad2/3
Zhou et al., J Allergy Clin Immunol 2007 (Asthma...) : These increases occur as TGF-beta1 downregulates IL-13 induced phosphoinositide-3 kinase activation while leaving the positive effect of IL-13 induced ERK on Smad signaling
Villar et al., Int J Cancer 2010 : The stable ectopic expression of Spred2 in PDV cells (SP cells) led to the loss of ERK 1,2 activation by TGF-beta1, although Smad2 activation was not affected, and the knockdown of Spred2 enhanced the activation of ERK1,2 signal by TGF-beta1
Heger et al., J Cell Physiol 2010 (Cardiomegaly...) : Specific inhibitors of PI3K ( 10 microM LY290042 or 10 nM wortmannin ) or ERK ( 10 microM PD98059 ) also blocked GDF15 induced hypertrophy and SMAD activation
Jiang et al., Int J Mol Med 2010 (MAP Kinase Signaling System) : We found that U0126, a specific inhibitor of ERK1/2 , and SB203580, a specific inhibitor of p38, down-regulated the TGF-beta1 induced phosphorylation of Smad2 at both linker and C-terminal sites in rat mesangial cells
Iwayama et al., Nephron extra 2011 : An inhibitor of ERK , PD98059, prevented CyA induced nuclear translocation of Smad2/3 and apoptosis
Nagasawa et al., J Surg Res 2013 (Aortic Aneurysm, Thoracic...) : Moreover, exogenous AngII resulted in increases in Smad2 activation and MMP-9 production, in an ERK dependent manner