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RHOA — TP53
Pathways - manually collected, often from reviews:
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
Xia et al., Nature structural & molecular biology 2007
(Neoplasms) :
Our analysis indicates that Ras ( V12 ) and loss of
p53 synergistically
induce RhoA activity, revealing a previously unknown role for p53 in tumor suppression ...
p53 prevents activation of
RhoA and thus induction of cell motility by Ras ( V12 ) through a simple signaling circuit, which integrates multiple inputs that converge on RhoA