◀ Back to MAPK14
CDH1 — MAPK14
Pathways - manually collected, often from reviews:
Text-mined interactions from Literome
Reddy et al., Mol Endocrinol 2005
(MAP Kinase Signaling System...) :
Akt activation is mediated through the activation of phosphatidylinositol 3 kinase, and both Akt and
MAPK activation are
mediated by an
E-cadherin adhesion induced ligand independent activation of epidermal growth factor receptor
Huan et al., J Biol Chem 2005
(Carcinoma...) :
Chromatin precipitation analyses and E-cadherin promoter reporter gene assays revealed that
E-cadherin induction by TFE3 or TFEB was primarily or exclusively direct and
mitogen activated protein kinase dependent in those cell types
Ordóñez-Morán et al., J Cell Biol 2008
(Colonic Neoplasms) :
As shown by the use of chemical inhibitors, dominant negative mutants and small interfering RNA, RhoA-ROCK, and
p38MAPK-MSK1 activation is
necessary for the induction of
CDH1/E-cadherin , CYP24, and other genes and of an adhesive phenotype by 1,25 ( OH ) ( 2 ) D ( 3 ) ... As shown by the use of chemical inhibitors, dominant negative mutants and small interfering RNA, RhoA-ROCK, and
p38MAPK-MSK1 activation is
necessary for the induction of
CDH1/E-cadherin , CYP24, and other genes and of an adhesive phenotype by 1,25 ( OH ) ( 2 ) D ( 3 )
Cheng et al., Mol Endocrinol 2010
(Ovarian Neoplasms) :
Furthermore, the
involvement of p38
MAPK in the down-regulation of
E-cadherin was confirmed using specific p38alpha MAPK small interfering RNA
Kolosova et al., J Cell Physiol 2011
:
However, neither Smad2/3 nor p38
MAPK were
required for the down-regulation of
E-cadherin , yet p38 MAPK was associated with fibronectin up-regulation ... However, neither Smad2/3 nor p38
MAPK were
required for the down-regulation of
E-cadherin , yet p38 MAPK was associated with fibronectin up-regulation
Tomlinson et al., PloS one 2012
:
MAPK activation
regulated migration and
E-cadherin expression, indicating that combined activation of PLC? and MAPK is required for a full EMT
Lau et al., PloS one 2013
(Neoplasm Invasiveness...) :
The pharmacological inhibition of phosphatidylinositol-3-kinase (PI3K), mammalian target of rapamycin (mTOR), and MEK suggests that both PI3K/Akt/mTOR and
MAPK/ERK signaling are
required for FGF2 induced
E-cadherin down-regulation