DNA double strand break repair via non-homologous end-joining

Anthony J. Davis, David J. Chen

Research output: Contribution to journalArticle

212 Citations (Scopus)

Abstract

DNA double-stranded breaks (DSB) are among the most dangerous forms of DNA damage. Unrepaired DSBs results in cells undergoing apoptosis or senescence whereas mis-processing of DSBs can lead to genomic instability and carcinogenesis. One important pathway in eukaryotic cells responsible for the repair of DSBs is non-homologous end-joining (NHEJ). In this review we will discuss the interesting new insights into the mechanism of the NHEJ pathway and the proteins which mediate this repair process. Furthermore, the general role of NHEJ in promoting genomic stability will be discussed.

Original languageEnglish (US)
Pages (from-to)130-143
Number of pages14
JournalTranslational Cancer Research
Volume2
Issue number3
DOIs
StatePublished - Jun 1 2013

Fingerprint

Double-Stranded DNA Breaks
Genomic Instability
Eukaryotic Cells
DNA Damage
Carcinogenesis
Apoptosis
1,2-di-(4-sulfamidophenyl)-4-butylpyrazolidine-3,5-dione
Proteins

Keywords

  • DNA double strand breaks
  • DNA-Ligase IV
  • DNA-PKcs
  • Ku70/80
  • Non-homologous end-joining
  • XLF
  • XRCC4

ASJC Scopus subject areas

  • Oncology
  • Radiology Nuclear Medicine and imaging
  • Cancer Research

Cite this

DNA double strand break repair via non-homologous end-joining. / Davis, Anthony J.; Chen, David J.

In: Translational Cancer Research, Vol. 2, No. 3, 01.06.2013, p. 130-143.

Research output: Contribution to journalArticle

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