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RAC1 — TP53

Text-mined interactions from Literome

Guo et al., Oncogene 2004 : We found that in primary MEFs ( 1 ) p53 or p19Arf deficiency led to a marked increase in the number of focal adhesion plaques and fibronectin production, and RhoA, Rac1 and Cdc42 contribute to the p53- and p19Arf mediated focal adhesion regulation, but not fibronectin synthesis ; ( 2 ) although endogenous Rac1 activity was required for the p19Arf or p53 deficiency induced migration phenotype, hyperactive Rho GTPases could not further enhance cell migration, rather they suppressed cell-cell adhesion of p53-/- MEFs ; ( 3 ) expression of the active mutant of RhoA, Rac1 or Cdc42, but not Ras, promoted an invasion phenotype of p53-/-, not p19Arf-/-, cells ; ( 4 ) although ROCK activation can partially recapitulate Rho induced invasion phenotype, multiple pathways regulated by RhoA, in addition to ROCK, are required to fully cooperate with p53 deficiency to promote cell invasion ; and ( 5 ) extracellular proteases produced by the active RhoA transduced cells are also required for the invasion phenotype of p53-/- cells
Xue et al., Int J Cancer 2006 (Carcinoma, Hepatocellular...) : Role of Rac1 and Cdc42 in hypoxia induced p53 and von Hippel-Lindau suppression and HIF1alpha activation
Debidda et al., J Biol Chem 2006 : Finally, phospho-Ser ( 15 ) p53 was significantly increased in L61Rac1 and Rac1 ( -/- ) cells, and genetic deletion of p53 from these cells readily reversed the senescence phenotype, indicating that Rac1 is functionally dependent on p53 in regulating cell senescence