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Ku DNA end-binding protein modulates homologous repair of double-strand breaks in mammalian cells.

Chromosomal double-strand breaks (DSBs) in mammalian cells are repaired by either homology-directed repair (HDR), using a homologous sequence as a repair template, or nonhomologous end-joining (NHEJ), which often involves sequence alterations at the DSB site. To characterize the interrelationship of these two pathways, we analyzed HDR of a DSB in cells deficient for NHEJ components. We find that the HDR frequency is enhanced in Ku70(-/-), XRCC4(-/-), and DNA-PKcs(-/-) cells, with the increase being particularly striking in Ku70(-/-) cells. Neither sister-chromatid exchange nor gene-targeting frequencies show a dependence on these NHEJ proteins. A Ku-modulated two-ended versus one-ended chromosome break model is presented to explain these results.

Pubmed ID: 11751629


  • Pierce AJ
  • Hu P
  • Han M
  • Ellis N
  • Jasin M


Genes & development

Publication Data

December 15, 2001

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM54688
  • Agency: NCI NIH HHS, Id: R01 CA085867
  • Agency: NCI NIH HHS, Id: R01 CA085867-01A2

Mesh Terms

  • Animals
  • Antigens, Nuclear
  • Cell Line
  • Cloning, Molecular
  • DNA
  • DNA Damage
  • DNA Helicases
  • DNA Primers
  • DNA Repair
  • DNA-Activated Protein Kinase
  • DNA-Binding Proteins
  • Gene Targeting
  • Humans
  • Mice
  • Mice, Knockout
  • Mutation
  • Nuclear Proteins
  • Polymerase Chain Reaction
  • Recombination, Genetic
  • Sister Chromatid Exchange
  • Transcription Factors