ATM stabilizes DNA double-strand-break complexes during V(D)J recombination

Andrea L. Bredemeyer, Girdhar G. Sharma, Ching-Yu Huang, Beth A. Helmink, Laura M. Walker, Katrina C. Khor, Beth Nuskey, Kathleen E. Sullivan, Tej K. Pandita, Craig H. Bassing and Barry P. Sleckman ()
Additional contact information
Andrea L. Bredemeyer: Washington University School of Medicine
Girdhar G. Sharma: Washington University School of Medicine
Ching-Yu Huang: Washington University School of Medicine
Beth A. Helmink: Washington University School of Medicine
Laura M. Walker: Washington University School of Medicine
Katrina C. Khor: Washington University School of Medicine
Beth Nuskey: University of Pennsylvania School of Medicine
Kathleen E. Sullivan: University of Pennsylvania School of Medicine
Tej K. Pandita: Washington University School of Medicine
Craig H. Bassing: University of Pennsylvania School of Medicine
Barry P. Sleckman: Washington University School of Medicine

Nature, 2006, vol. 442, issue 7101, 466-470

Abstract: Examination of the role of the ATM protein in oncogenic chromosomal translocations in the disease ataxia telangiectasia finds that ATM is involved directly in stabilizing a complex that occurs when DNA double-strand breaks are made in lymphocyte antigen receptor loci. When the complex is not stabilized, the DNA ends are able to undergo aberrant reactions that can lead to translocations.

Date: 2006
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DOI: 10.1038/nature04866

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