More p53 (green) is cytoplasmic when K320 is acetylated (bottom).
The stabilization of p53 following cellular damage can trigger either apoptosis or a reversible cell cycle checkpoint that probably gives cells time to recover. As either savior or killer, p53 is subject to a battery of posttranslational modifications, including phosphorylation and acetylation. One such acetylation event (on K373) is now shown to trigger apoptosis, whereas another (on K320) works against death.
To understand how, the authors expressed mutant versions of p53 that mimic the acetylation events. After a brief treatment with a mild DNA-damaging agent, only cells with K320-modified p53 resumed proliferation; the rest died. The promoters bound, and genes activated, by the two p53...
