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EPHB2 — SMAD3

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 )
Hayashida et al., FASEB J 2003 (MAP Kinase Signaling System) : In a heterologous DNA binding transcription assay, biochemical or dominant negative ERK blockade reduced TGF-beta1 induced Smad3 activity ... 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
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
Matsuura et al., Biochemistry 2005 : We further show that mutation of the ERK phosphorylation sites increases the ability of Smad3 to stimulate a Smad target gene, suggesting that ERK phosphorylation inhibits Smad3 activity
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 : In addition, the inhibition of ERK1/2 activity with MEK1/2 inhibitor U0126 increased TGF-beta mediated phosphorylation of Smad3 ... 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
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
Kim et al., Cancer Lett 2012 (Breast Neoplasms) : Interestingly, EGF induced smad3 phosphorylation was completely blocked by smad7 over-expression, but not the phosphorylation of ERK and JNK
Iwayama et al., Nephron extra 2011 : An inhibitor of ERK , PD98059, prevented CyA induced nuclear translocation of Smad2/3 and apoptosis
Suwanabol et al., J Vasc Surg 2012 : Overexpression of the signaling protein Smad3 enhanced TGF-ß induced activation of ERK MAPK, whereas inhibition of Smad3 with a siRNA blocked ERK MAPK phosphorylation in response to TGF-ß