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Nature Cell Biology 2, E215 - E217 (2000)
doi:10.1038/35046628
An unlikely player joins the ATM signalling network
Martin F. Lavin1
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Martin F Lavin has a joint appointment at the Queensland
Institute of Medical Research and the University of Queensland,
Brisbane, Australia.
e-mail: martinL@qimr.edu.au
Abstract
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.
