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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