Under normal conditions, p53 is kept at low levels in the cell by its negative regulator, MDM2, which targets it for degradation. However, upon exposure to DNA-damaging agents or stress, p53 is stabilized and accumulates in the cell. This stabilization occurs through post-translational modifications, such as phosphorylation and acetylation, which inhibit its interaction with MDM2. As a result, p53 can translocate to the nucleus and activate the transcription of genes involved in cell cycle arrest and apoptosis.
