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

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

62 Scopus citations

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).

Original languageEnglish (US)
Pages (from-to)1-8
Number of pages8
JournalRadiation Research
Volume181
Issue number1
DOIs
StatePublished - Jan 2014

ASJC Scopus subject areas

  • Biophysics
  • Radiation
  • Radiology Nuclear Medicine and imaging

Fingerprint Dive into the research topics of 'Role of 53BP1 in the regulation of DNA double-strand break repair pathway choice'. Together they form a unique fingerprint.

Cite this