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MAPK3 — SMAD1
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Wrana et al., Science's STKE : signal transduction knowledge environment 2000
:
In the cytosol,
Smad translocation might be
inhibited by
mitogen activated protein kinase dependent phosphorylation, whereas in the nucleus Smads interact with a number of transcription factors that themselves are primary targets of other signaling pathways
Lee et al., Int J Oncol 2004
(Stomach Neoplasms) :
In this study, we examined effects of cell adhesion status on the TGF-beta1 mediated
Erk1/2 regulation, and roles of
Smad proteins on the cell adhesion
mediated effects, using a gastric carcinoma cell variant
Kano et al., Endocrinology 2005
:
BMPs
induced both
Smad1/5/8 phosphorylation and Tlx2-Luc activation, whereas activin stimulated 3TP-Luc activity and p38
MAPK phosphorylation
Zhao et al., Mol Cell Biochem 2008
(Fibrosis...) :
Additionally, the inhibition of
MAPK signaling
had no effect on
Smad activation elicited by chymase
Schievenbusch et al., Biochem Biophys Res Commun 2009
(Fibrosis) :
As previously shown,
Erk1/2 phosphorylation
results in
Smad-linker phosphorylation, thereby antagonizing cellular signals induced by TGFbeta
Zhu et al., Prostate 2010
(MAP Kinase Signaling System) :
These findings suggest a dual role for PHB as a downstream determinant of the cellular response to TGF-beta via
Smad dependent pathway ( apoptosis ) and
MAPK intracellular signaling ( survival )
Zhou et al., Dev Cell 2010
:
BMP2 induction of
Smad1/5/8 phosphorylation and Runx2 expression, but not noncanonical p38
MAPK activation , was reduced in chondrocytes from neogenin mutant mice
Rodrigues Díez et al., PloS one 2010
(Fibrosis) :
In cultured rat VSMCs, direct
AngII/Smad pathway activation was
mediated by p38
MAPK and ROCK activation
Ungefroren et al., Int J Oncol 2011
(Carcinoma, Pancreatic Ductal...) :
Biochemically, dnSrc inhibition failed to block TGF-ß1/ALK5 induced activation of Smad2 and Smad3, but partially
inhibited transcriptional activation of
TGF-ß/Smad-responsive reporter genes, and effectively blocked basal and TGF-ß1 induced activation of p38
MAPK