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Summary: Molecular Cell
Article
Essential Role for DNA-PKcs
in DNA Double-Strand Break Repair
and Apoptosis in ATM-Deficient Lymphocytes
Elsa Calle´ n,1,4,6 Mila Jankovic,2,4 Nancy Wong,1 Shan Zha,3 Hua-Tang Chen,1 Simone Difilippantonio,1 Michela Di Virgilio,2
Gordon Heidkamp,2 Frederick W. Alt,3 Andre´ Nussenzweig,1,5,* and Michel Nussenzweig2,5,*
1Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892, USA
2Laboratory of Molecular Immunology, the Rockefeller University and Howard Hughes Medical Institute, New York, NY 10065, USA
3Howard Hughes Medical Institute, Program in Cellular and Molecular Medicine, The Children's Hospital, and Department of Genetics,
Harvard Medical School, Boston, MA 02115, USA
4These authors contributed equally to this work
5These authors contributed equally to this work
6Present address: Department of Genetics and Microbiology, Universitat Autonoma de Barcelona, 08193 Bellaterra, Barcelona, Spain
*Correspondence: andre_nussenzweig@nih.gov (A.N.), nussen@mail.rockefeller.edu (M.N.)
DOI 10.1016/j.molcel.2009.04.025
SUMMARY
The DNA double-strand break (DSB) repair protein
DNA-PKcs and the signal transducer ATM are both
activated by DNA breaks and phosphorylate similar
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