Abstract

p53 plays a central role in the cellular response to DNA damage. Induction of this protein is triggered by DNA breaks and correlates with their presence (,). In addition, p53 is upregulated by a number of different stress conditions including hypoxia, oncogene activation, viral infection, and ribonucleotide depletion (reviewed in ()). The ability of C-terminal domain of p53 to bind DNA ends (,), insertion/deletion mismatches (), recombination intermediates () and gamma-irradiated DNA in vitro () implies that direct recognition of DNA lesions by p53 can play a role in its induction ().

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