The endless tale of non-homologous end-joining

Eric Weterings, David J. Chen

Research output: Contribution to journalReview articlepeer-review

287 Scopus citations


DNA double-strand breaks (DSBs) are introduced in cells by ionizing radiation and reactive oxygen species. In addition, they are commonly generated during V(D)J recombination, an essential aspect of the developing immune system. Failure to effectively repair these DSBs can result in chromosome breakage, cell death, onset of cancer, and defects in the immune system of higher vertebrates. Fortunately, all mammalian cells possess two enzymatic pathways that mediate the repair of DSBs: homologous recombination and non-homologous end-joining (NHEJ). The NHEJ process utilizes enzymes that capture both ends of the broken DNA molecule, bring them together in a synaptic DNA-protein complex, and finally repair the DNA break. In this review, all the known enzymes that play a role in the NHEJ process are discussed and a working model for the co-operation of these enzymes during DSB repair is presented.

Original languageEnglish (US)
Pages (from-to)114-124
Number of pages11
JournalCell Research
Issue number1
StatePublished - Jan 2008


  • ATM
  • Artemis
  • Cernunnos
  • DNA double-strand break
  • DNA-PK
  • DSB
  • Ku70/80
  • Ligase IV
  • NHEJ
  • Non-homologous end-joining
  • V(D)J recombination
  • XLF
  • XRCC4

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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