◀ Back to EPHB2

EPHB2 — SMAD1

Text-mined interactions from Literome

Mulder et al., Cytokine Growth Factor Rev 2000 (MAP Kinase Signaling System) : Our results provide evidence that Erk mediated phosphorylation of Smad1 in response to TGFbeta is critical for regulating Smad1 subcellular localization ; this may be a key determinant in maintaining TGFbeta dependent transcriptional activation
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 )
Althini et al., Mol Cell Neurosci 2004 (MAP Kinase Signaling System) : A reporter assay using NGF stimulated PC12 cells demonstrated that MEK/Erk/Elk-driven transcriptional activity was inhibited by Smad1/5 and by PD98059
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
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
Yang et al., Circ Res 2008 (Hypertension, Pulmonary...) : Furthermore, activation of ERK1/2 by platelet derived growth factor BB also caused Smad1 linker region phosphorylation and inhibited BMP4 induced Id1 gene expression
Trzeciakiewicz et al., J Agric Food Chem 2010 : Moreover, phosphorylation of Smad1/5/8 was enhanced by Hp7G, while ERK1/2 remained unchanged after 48 h. Hp7G decreased RANKL gene expression
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
Jun et al., J Biol Chem 2010 : Erk activation enhanced the association of Runx2 with p300 and Smad1
Park et al., Anticancer Drugs 2013 (Bone Neoplasms...) : Whereas BMP-2 mainly activated ERK1/2 , BMP-9 phosphorylated p38 within 1 h. pBMP-2 did not activate either the Smad or ERK/p38, whereas pBMP-9, like BMP-9, induced both Smad1/5/8 and p38 phosphorylation