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MAPK8 — RAC3
Pathways - manually collected, often from reviews:
-
KEGG Wnt signaling pathway:
RAC1/RAC2/RAC3
→
MAPK10/MAPK8/MAPK9
(protein-protein, activation)
-
KEGG Focal adhesion:
RAC1/RAC2/RAC3
→
MAPK10/MAPK8/MAPK9
(protein-protein, phosphorylation)
-
KEGG Pathways in cancer:
RAC1/RAC2/RAC3/RHOA
→
MAPK10/MAPK8/MAPK9
(protein-protein, indirect effect)
-
KEGG Colorectal cancer:
RAC1/RAC2/RAC3/RHOA
→
MAPK10/MAPK8/MAPK9
(protein-protein, activation)
Text-mined interactions from Literome
Mainiero et al., Immunity 2000
(MAP Kinase Signaling System) :
Finally, we provide direct evidence that p95 Vav and
Rac control the activation of p38
MAPK triggered by beta1 integrins
Versteeg et al., J Biol Chem 2000
:
In turn
Rac mediates p38
mitogen activated protein ( MAP ) kinase activation and cytoskeletal reorganization, whereas factor VIIa induced p42/p44 MAP kinase stimulation required PI3K enzymatic activity but was not inhibited by dominant negative Rac proteins
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
Chen et al., Mol Microbiol 2004
(MAP Kinase Signaling System) :
Co-expression of DARas with dominant active
Rac ( DARac )
stimulates MAPK activation and restores the wild-type phenotype
Nishida et al., J Biol Chem 2005
:
Dominant negative
Rac inhibited angiotensin II-stimulated ROS production, JNK activation, and p38
MAPK activation but did not affect ERK activation
Otis et al., Mol Cell Endocrinol 2007
:
The increase in cell protein content induced by Ang II entails formation of a cortical actin ring and
Rac dependent
activation of p42/p44(mapk) and p38
MAPK