The tumor suppressor gene p53 plays a major role in the protection of
cells from DNA damage. Activation of the protein in response to irradi
ation or genotoxic agents, and possibly by other signals, results in g
rowth arrest at the G1 phase of the cell cycle or in apoptosis. While
it has been shown that the ability of p53 to function as a sequence-sp
ecific transcriptional activator is necessary for the induction of gro
wth arrest, the mechanism of p53-mediated apoptosis is not clear yet.
It appears that under some conditions activation of the G1 checkpoint
will prevent apoptosis, but cellular environment may alter the result
of p53 activation towards cell death. p53 may also directly induce apo
ptosis through several pathways, which may be transcriptionally depend
ent or independent. The outcome -a G1 arrest or apoptosis -will depend
on a complex network of regulatory signals.