A PROTEIN that is synthesized after the infliction of DNA damage, p53 has been called the guardian of the genome.1 It is associated with sites of DNA damage and causes cell-cycle arrest at the G1 phase until the DNA damage has been repaired. Once the damage is repaired, p53 is degraded. This function is lost in approximately 50% of human tumors in which p53 is inactivated by a mutation in its gene or by the binding of proteins encoded by viral or cellular oncogenes.2 Deleterious p53 mutations, usually found in the DNA-binding region of the protein, reduce the capacity of p53 to bind to damaged sites; as a result, replication occurs with reduced fidelity, leading to cell transformations and cancer.
Gasparro FP. p53 in Dermatology. Arch Dermatol. 1998;134(8):1029–1032. doi:https://doi.org/10.1001/archderm.134.8.1029
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