Individuals with the hereditary disorder ataxia telangiectasia suffer from neurodegeneration, immunodeficiency, and an increased incidence of cancer. The genetic basis for ataxia telangiectasia is a loss-of-function mutation in the gene encoding ATM (ATM; ataxia telangiectasia mutated). Besides p53, what other substrate is phosphorylated by ATM? How does the phosphorylation of this substrate lead to inactivation of CDKs to enforce cell cycle arrest?

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