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9 December 2013 Role of 53BP1 in the Regulation of DNA Double-Strand Break Repair Pathway Choice
Arun Gupta, Clayton R. Hunt, Sharmistha Chakraborty, Raj K. Pandita, John Yordy, Deepti B. Ramnarain, Nobuo Horikoshi, Tej K. Pandita
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Abstract

The p53-binding protein 1 (53BP1) is a well-known DNA damage response (DDR) factor, which is recruited to nuclear structures at the site of DNA damage and forms readily visualized ionizing radiation (IR) induced foci. Depletion of 53BP1 results in cell cycle arrest in G2/M phase as well as genomic instability in human as well as mouse cells. Within the DNA damage response mechanism, 53BP1 is classified as an adaptor/mediator, required for processing of the DNA damage response signal and as a platform for recruitment of other repair factors. More recently, specific 53BP1 contributions to DSB repair pathway choice have been recognized and are being characterized. In this review, we have summarized recent advances in understanding the role of 53BP1 in regulating DNA DSBs repair pathway choice, variable diversity joining [V(D)J] recombination and class-switch recombination (CSR).

Arun Gupta, Clayton R. Hunt, Sharmistha Chakraborty, Raj K. Pandita, John Yordy, Deepti B. Ramnarain, Nobuo Horikoshi, and Tej K. Pandita "Role of 53BP1 in the Regulation of DNA Double-Strand Break Repair Pathway Choice," Radiation Research 181(1), 1-8, (9 December 2013). https://doi.org/10.1667/RR13572.1
Received: 8 October 2013; Accepted: 1 November 2013; Published: 9 December 2013
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