atm and p53 cooperate in apoptosis and suppression of tumorigenesis, but not in resistance to acute radiation toxicity

Abstract

Mutations in atm and p53 cause the human cancer-associated diseases ataxia-telangiectasia1 and Li-Fraumeni syndrome2,3, respectively. The two genes are believed to interact in a number of pathways4–6, including regulation of DNA damage–induced cell-cycle checkpoints7, apoptosis and radiation sensitivity8, and cellular proliferation9. Atm-null mice10–12, as… (More)
DOI: 10.1038/ng0897-397

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