Abstract

Genome maintenance is a constant concern for cells, and a coordinated response to DNA damage is required to maintain cellular viability and prevent disease. The ataxia-telangiectasia mutated (ATM) and ATM and RAD3-related (ATR) protein kinases act as master regulators of the DNA-damage response by signalling to control cell-cycle transitions, DNA replication, DNA repair and apoptosis. Recent studies have provided new insights into the mechanisms that control ATR activation, have helped to explain the overlapping but non-redundant activities of ATR and ATM in DNA-damage signalling, and have clarified the crucial functions of ATR in maintaining genome integrity.

Author affiliations

1. Department of Chemical and Systems Biology, Stanford University School of Medicine, Clark Center, 318 Campus Drive, W350B, Stanford, California 94305-5441, USA.
   Email: cimprich@stanford.edu
2. Department of Biochemistry, Vanderbilt University School of Medicine, 613 Light Hall, 23rd @ Pierce Avenue, Nashville, Tennesee 37232, USA.
   Email: david.cortez@vanderbilt.edu

Published online 2 July 2008

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