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• W2022163673 endingPage "12435" @default.
• W2022163673 startingPage "12430" @default.
• W2022163673 abstract "Nonhomologous end joining (NHEJ), a form of DNA double-strand break (DSB) repair, is conserved from bacteria to humans. One essential NHEJ factor is Ku, which consists of a heterodimer of Ku70 and Ku86. In a plethora of model systems, null mutations for Ku70 or Ku86 present with defects in DNA DSB repair, variable(diversity)joining [V(D)J] recombination, and/or telomere maintenance. The complete loss of Ku from bacteria to mice is, however, compatible with viability. In striking contrast, human patients with mutations of either Ku subunit have never been described. Here, we have used recombinant adeno-associated virus-mediated gene targeting to produce a human somatic cell line that expresses a conditionally null allele of Ku86. The induced loss of Ku86 results in cell death accompanied by massive telomere loss in the form of t-circles. Thus, Ku86 is an essential gene in human somatic cells because of its requirement, not in NHEJ or V(D)J recombination, but in telomere maintenance." @default.
• W2022163673 created "2016-06-24" @default.
• W2022163673 creator A5003620789 @default.
• W2022163673 creator A5004352007 @default.
• W2022163673 creator A5066373462 @default.
• W2022163673 date "2009-07-28" @default.
• W2022163673 modified "2023-09-27" @default.
• W2022163673 title "Ku86 represses lethal telomere deletion events in human somatic cells" @default.
• W2022163673 cites W1972313386 @default.
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• W2022163673 doi "https://doi.org/10.1073/pnas.0903362106" @default.
• W2022163673 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/2718384" @default.
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• W2022163673 hasPublicationYear "2009" @default.
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