ATM, the product of the gene that is mutated in the human genetic disorder ataxia telangiectasia (A-T), responds to DNA damage by phosphorylating several key substrates that are involved in both the sensing of damage and the activation of cell-cycle checkpoints. The unexpected activation of ATM kinase in response to insulin supports a more general signalling role for this enzyme.
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Lavin, M. An unlikely player joins the ATM signalling network. Nat Cell Biol 2, E215–E216 (2000). https://doi.org/10.1038/35046628
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DOI: https://doi.org/10.1038/35046628
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