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Radiation-induced Assembly of Rad51 and Rad52 Recombination Complex Requires ATM and c-Abl

Chen, Gang and Yuan, Shyng-Shiou F. and Liu, Wei and Xu, Yang and Trujillo, Kelly and Song, Binwei and Cong, Feng and Goff, Stephen P. and Wu, Yun and Arlinghaus, Ralph and Baltimore, David and Gasser, Paul J. and Park, Min S. and Sung, Patrick and Lee, Eva Y.-H. P. (1999) Radiation-induced Assembly of Rad51 and Rad52 Recombination Complex Requires ATM and c-Abl. Journal of Biological Chemistry, 274 (18). pp. 12748-12752. ISSN 0021-9258. doi:10.1074/jbc.274.18.12748.

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Cells from individuals with the recessive cancer-prone disorder ataxia telangiectasia (A-T) are hypersensitive to ionizing radiation (I-R). ATM (mutated in A-T) is a protein kinase whose activity is stimulated by I-R. c-Abl, a nonreceptor tyrosine kinase, interacts with ATM and is activated by ATM following I-R. Rad51 is a homologue of bacterial RecA protein required for DNA recombination and repair. Here we demonstrate that there is an I-R-induced Rad51 tyrosine phosphorylation, and this induction is dependent on both ATM and c-Abl. ATM, c-Abl, and Rad51 can be co-immunoprecipitated from cell extracts. Consistent with the physical interaction, c-Abl phosphorylates Rad51 in vitro and in vivo. In assays using purified components, phosphorylation of Rad51 by c-Abl enhances complex formation between Rad51 and Rad52, which cooperates with Rad51 in recombination and repair. After I-R, an increase in association between Rad51 and Rad52 occurs in wild-type cells but not in cells with mutations that compromise ATM or c-Abl. Our data suggest signaling mediated through ATM, and c-Abl is required for the correct post-translational modification of Rad51, which is critical for the assembly of Rad51 repair protein complex following I-R.

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Baltimore, David0000-0001-8723-8190
Additional Information:© 1999 by The American Society for Biochemistry and Molecular Biology, Inc. (Received for publication, February 24, 1999) Anti-Rad51 antibody used in initial studies was kindly provided by Dr. T. Ogawa at the Osaka University, and the Rad51 expression plasmid was supplied by Drs. W.-H. Lee and P.-L Chen. We thank Drs. Gopal K. Dasika and Hao-Chi Hsu for helping with site-specific mutagenesis and providing GST-c-Abl protein, respectively. Critical reading by Drs. Alan Tomkinson, Steve Skapek, McGreggor Crowley, and John Leppard is greatly appreciated. This work was supported by grants from Ataxia Telangiectasia Children's Project and National Institutes of Health Grant 1R01NS378381-01 (to E.L.). The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. The first two authors contributed equally to this work. [G.C. was a] [r]ecipient of National Institutes of Health Postdoctoral Fellowship.
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Ataxia TelangiectasiaUNSPECIFIED
NIH Postdoctoral FellowshipUNSPECIFIED
Issue or Number:18
Record Number:CaltechAUTHORS:CHEjbc99
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ID Code:6857
Deposited By: Archive Administrator
Deposited On:29 Dec 2006
Last Modified:08 Nov 2021 20:37

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