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Genes Dev. 2001 Dec 15;15(24):3237-42.

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

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1
Cell Biology Program, Memorial Sloan-Kettering Cancer Center, and Cornell University Graduate School of Medical Sciences, New York, New York 10021, USA.

Abstract

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.

PMID:
11751629
PMCID:
PMC312854
DOI:
10.1101/gad.946401
[Indexed for MEDLINE]
Free PMC Article
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