摘要
The p53 protein is mutated or inactivated in more than 50% of human cancers, underscoring its cardinal importance as an oncosuppressor, p53 is expressed in all nucleated cells and can be activated by a plethora of post-transcriptional modifications （in particular by the phosphorylation of critical serine residues）, as well as by the inhibition of its degradation （mainly mediated by the E3 ubiquitin ligase MDM2）. p53 was first characterized as a transcription factor that, once activated, drives the expression of gene programs causing a transient cell cycle arrest linked to DNA repair, a permanent and irreversible cell cycle arrest （senescence） or programmed cell death by apoptosis.
