title: Role of 53BP1 in the regulation of DNA double-strand break repair pathway choice.
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).
authors: Department of Radiation Oncology, University of Texas Southwestern Medical Center, Dallas, Texas 75390.
authors: Arun
authors: A
authors: Gupta
authors: Clayton R
authors: CR
authors: Hunt
authors: Sharmistha
authors: S
authors: Chakraborty
authors: Raj K
authors: RK
authors: Pandita
authors: John
authors: J
authors: Yordy
authors: Deepti B
authors: DB
authors: Ramnarain
authors: Nobuo
authors: N
authors: Horikoshi
authors: Tej K
authors: TK
authors: Pandita
mesh_terms: D000818:Animals; D053903:DNA Breaks, Double-Stranded; D004260:DNA Repair; D006801:Humans; D047908:Intracellular Signaling Peptides and Proteins / Q000737:chemistry / Q000378:metabolism*; D060152:V(D)J Recombination
chemical_list: D047908:Intracellular Signaling Peptides and Proteins