Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA damage involves Cdk5 mediated phosphorylation of Ser-794 followed by autophosphorylation at Ser-1891. Active ATM kinase regulates a number of proteins involved in cell cycle checkpoint control, apoptosis and DNA repair. The Cdk5-ATM pathway regulates phosphorylation and function of the ATM targets p53 and H2AX in postmitotic neurons. Other known substrates of ATM include Chk2, Chk1, CtIP, 4E-BP1, BRCA1, RPA3, SMC1, FANCD2, Rad17, Artemis, Nbs1, and the I-2 regulatory subunit of PP1. Thus, activation of Cdk5 by DNA damage may be an important initiator of ATM-dependent regulation of cell cycle checkpoints.
Ataxia telangiectasia mutated kinase (ATM) is a serine/threonine kinase that regulates cell cycle checkpoints and DNA repair. Mutations of ATM cause a spectrum of defects ranging from neurodegeneration to cancer predisposition. Activation of ATM after DNA
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