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CDC42 — JUN

Text-mined interactions from Literome

Li et al., J Clin Invest 1999 : Although both Cdc42 and Rho were involved in the shear stress induced transcription factor AP-1 acting on the 12-O-tetradecanoyl-13-phorbol-acetate-responsive element ( TRE ), only Cdc42 was sufficient to activate AP-1/TRE ... Dominant negative mutants of Cdc42 and Rho, as well as recombinant C3 exoenzyme, attenuated the shear stress activation of c-Jun NH2-terminal kinases (JNKs), suggesting that Cdc42 and Rho regulate the shear stress induction of AP-1/TRE activity through JNKs. Shear stress induced cell alignment and stress fiber formation were inhibited by the dominant negative mutants of Rho and p160ROCK, but not by the dominant negative mutant of Cdc42, indicating that the Rho-p160ROCK pathway regulates the cytoskeletal reorganization in response to shear stress
Kaminuma et al., Mol Cell Biol 2001 : On the other hand, Vav induced the activation of Rac1 or Cdc42 and c-Jun N-terminal kinase (JNK), enhanced the transcriptional and DNA binding activities of AP-1, and induced increased phosphorylation of c-Jun
Miyamoto et al., J Biol Chem 2004 (MAP Kinase Signaling System) : Taken together, these results suggest that the endothelin A receptor transduces the signal of inhibition of cell migration through Cdc42 dependent c-Jun N-terminal kinase activation by using Nck1
Su et al., Carcinogenesis 2005 : Expression of a mutant Cdc42 ( N17 Cdc42 ) dramatically reduced resveratrol induced c-Jun N-terminal kinase activity, FasL expression and apoptotic cell death
Bagrodia et al., J Biol Chem 1995 : Both, activated ( GTPase-defective ) Cdc42 and a constitutively active PAK-3 mutant stimulated the activity of Jun kinase 1 (JNK1) in transfected cells
Bazenet et al., Proc Natl Acad Sci U S A 1998 : Cdc42 activation produced an increase in the level of c-Jun and of its phosphorylation
Li et al., J Biol Chem 1998 : Fibroblast transformation by Fps/Fes tyrosine kinases requires Ras, Rac, and Cdc42 and induces extracellular signal regulated and c-Jun N-terminal kinase activation ... Ras controls the activation of extracellular signal regulated kinases ( ERKs ), while Rac and Cdc42 regulate the c-Jun N-terminal kinases (JNKs)
Levi et al., Mol Endocrinol 1998 : Stimulation of Jun N-terminal kinase (JNK) by gonadotropin releasing hormone in pituitary alpha T3-1 cell line is mediated by protein kinase C, c-Src, and CDC42