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Science 294 (5547): 1713-1716

Copyright © 2001 by the American Association for the Advancement of Science

ATR and ATRIP: Partners in Checkpoint Signaling

David Cortez,12 Saritha Guntuku,12 Jun Qin,13 Stephen J. Elledge124*

The checkpoint kinases ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3 related) transduce genomic stress signals to halt cell cycle progression and promote DNA repair. We report the identification of an ATR-interacting protein (ATRIP) that is phosphorylated by ATR, regulates ATR expression, and is an essential component of the DNA damage checkpoint pathway. ATR and ATRIP both localize to intranuclear foci after DNA damage or inhibition of replication. Deletion of ATR mediated by the Cre recombinase caused the loss of ATR and ATRIP expression, loss of DNA damage checkpoint responses, and cell death. Therefore, ATR is essential for the viability of human somatic cells. Small interfering RNA directed against ATRIP caused the loss of both ATRIP and ATR expression and the loss of checkpoint responses to DNA damage. Thus, ATRIP and ATR are mutually dependent partners in cell cycle checkpoint signaling pathways.

1 Verna and Mars McLean Department of Biochemistry and Molecular Biology,
2 Howard Hughes Medical Institute,
3 Department of Cell Biology,
4 Department of Molecular and Human Genetics, Baylor College of Medicine, One Baylor Plaza, Houston, TX 77030, USA.
*   To whom correspondence should be addressed.


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The Rad9-Hus1-Rad1 Checkpoint Clamp Regulates Interaction of TopBP1 with ATR.
J. Lee, A. Kumagai, and W. G. Dunphy (2007)
J. Biol. Chem. 282, 28036-28044
   Abstract »    Full Text »    PDF »
The Mre11-Rad50-Nbs1 Complex Acts Both Upstream and Downstream of Ataxia Telangiectasia Mutated and Rad3-related Protein (ATR) to Regulate the S-phase Checkpoint following UV Treatment.
E. Olson, C. J. Nievera, A. Y.-L. Lee, L. Chen, and X. Wu (2007)
J. Biol. Chem. 282, 22939-22952
   Abstract »    Full Text »    PDF »
Cyclin-Dependent Kinase 2 Dependent Phosphorylation of ATRIP Regulates the G2-M Checkpoint Response to DNA Damage.
J. S. Myers, R. Zhao, X. Xu, A.-J. L. Ham, and D. Cortez (2007)
Cancer Res. 67, 6685-6690
   Abstract »    Full Text »    PDF »
Nonhomologous End Joining Is Essential for Cellular Resistance to the Novel Antitumor Agent, {beta}-Lapachone.
M. S. Bentle, K. E. Reinicke, Y. Dong, E. A. Bey, and D. A. Boothman (2007)
Cancer Res. 67, 6936-6945
   Abstract »    Full Text »    PDF »

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