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First published online December 22, 2004
doi: 10.1242/10.1242/jcs.01626

Journal of Cell Science 118, 1-6 (2005)
Published by The Company of Biologists 2005
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G2 damage checkpoints: what is the turn-on?

Matthew J. O'Connell1,* and Karlene A. Cimprich2

1 Department of Oncological Sciences, Mount Sinai School of Medicine, One Gustave L. Levy Place, Box 1130, New York, NY 10029, USA
2 Stanford University, Department of Molecular Pharmacology, 318 Campus Drive, Stanford, CA 94305, USA



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  		Fig. 1. The G2 DNA damage checkpoint. In response to DNA damage, or agents that block replication, checkpoint complexes consisting of (1) Rad17 and Rfc2-5, (2) Rad9, Rad1 and Hus1, and (3) ATR and ATRIP are recruited to the damaged region. Together with mediator proteins, ATR then activates Chk1 by phosphorylation to promote a blockade to Cdc2/Cyclin B activation, and thus cells are unable to enter mitosis.

 


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  		Fig. 2. Model for replication-dependent ATR activation. When a polymerase encounters a lesion (shown here on the leading strand), the polymerase is slowed while the minichromosome maintenance (MCM) helicase continues to unwind the duplex DNA. This leads to accumulation of single-stranded DNA on the leading and/or lagging strand and recruitment of RPA and polymerase {alpha}. The ATR-ATRIP complex and the 9-1-1 complex are then recruited to the ssDNA. Phosphorylation and activation of Chk1 follows and is mediated by claspin and/or additional mediator proteins.

 




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