Activation of the p53 tumor suppressor protects organisms from propagation of cells that carry damaged DNA with potentially oncogenic mutations. Following cellular stress, p53 is stabilized and activated to transcribe a large number of genes that regulates cell-cycle arrest, DNA repair, or apoptosis. The transacting activity of p53 is driven by its sequence-specific DNA-binding domain. Since the potential p53-binding sites in the human genome are among 300-1600, gene-transcription specificity is thought to be modulated through a complex pattern of protein-protein interactions as well as posttranslational modifications. An increasing number of p53 interacting proteins is being described which modulate p53 activity in normal as in cancer cells. Here, we highlight how through specific interactions and modifications p53 protein exerts its biological activity.
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