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CDC42 — MAPK8
Pathways - manually collected, often from reviews:
-
BioCarta agrin in postsynaptic differentiation:
cdc42 (CDC42)
→
JNK1 (MAPK8)
(modification, activates)
-
NCI Pathway Database N-cadherin signaling events:
RAC1-CDC42/GTP complex (RAC1_CDC42)
→
JNK1 (MAPK8)
(modification, activates)
Meriane et al., Mol Biol Cell 2000, Charrasse et al., J Cell Biol 2002
Evidence: mutant phenotype, assay, other species
-
NCI Pathway Database ErbB2/ErbB3 signaling events:
JNK family (MAPK8/MAPK9/MAPK10)
→
RAC1-CDC42/GTP complex (RAC1_CDC42)
(modification, collaborate)
Yamauchi et al., J Cell Biol 2008
Evidence: mutant phenotype, assay
-
NCI Pathway Database Endothelins:
Rho Family GTPase-active (RHOA/CDC42/RAC1)
→
JNK1 (MAPK8)
(modification, activates)
Arai et al., Mol Pharmacol 2003, Nishida et al., J Biol Chem 2007, Yogi et al., Arterioscler Thromb Vasc Biol 2007
Evidence: mutant phenotype
Text-mined interactions from Literome
Philips et al., J Biol Chem 2000
:
Surprisingly, the ability of
Cdc42 to
induce p38
MAPK activity in suspended mouse embryonic fibroblast was impaired
Arozarena et al., J Biol Chem 2000
:
Moreover, we show that the potentiating effect of ionomycin on Ras-GRF mediated
MAPK stimulation is also
regulated by
Cdc42
Rul et al., Ann N Y Acad Sci 2002
(MAP Kinase Signaling System) :
Here, we describe that the inhibition of Rac1 or
Cdc42 signaling
leads to
MAPK ERK activation via a pathway involving PI(3)K, Akt, Raf, and MEK, but not Ras
Zhong et al., Blood 2003
(MAP Kinase Signaling System) :
Rac and
Cdc42 , but not Ras or Rho, were
responsible for this
MAPK/ERK activation ... We conclude from these data that
Rac/Cdc42 dependent
activation of
MAPK/ERK is a critical event in the immediate phagocytic response of PMNs to microbial challenge
Shi et al., J Immunol 2003
(MAP Kinase Signaling System) :
Mechanistically, a small GTPase
Cdc42 failed to be activated after TR6 pretreatment of human T cells, and further downstream, p38
mitogen activated protein kinase activation, actin polymerization, and pseudopodium formation were all
down-regulated in the treated T cells
Stepan et al., Am J Physiol Gastrointest Liver Physiol 2004
:
In contrast, G17 stimulated
MAPK activation was
blocked by > 80 % by dominant negative Ras but not by dominant negative Rho and
Cdc42
Szczur et al., Blood 2006
(MAP Kinase Signaling System) :
We further suggest that CDC42GAP mediated extracellular signal regulated kinase ( ERK ) activity regulates motility associated with podosome-like structures at the cell leading edge, while
CDC42GAP induced p38 (
MAPK ) phosphorylation regulates directed migration by antagonizing filopodia assembly
Yano et al., Circ Res 2007
(Inflammation) :
However, DN-RhoA and
DN-Cdc42 activated p38
MAPK , but not ERK1/2
Tobe et al., Cell division 2009
:
It was found that Swe1 mediated inhibitory tyrosine phosphorylation of
Cdc28 during filamentous growth is in part
mediated by Ras2 activation of PKA, but not
Kss1-MAPK , signaling