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

Genes & development | Dec 15, 2001

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 RIS Download

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 | Ku Autoantigen | Mice | Mice, Knockout | Mutation | Nuclear Proteins | Polymerase Chain Reaction | Recombination, Genetic | Sister Chromatid Exchange | Transcription Factors

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Associated grants

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

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