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Letter
Nature Cell Biology 8, 885–890 (1 August 2006) | doi:10.1038/ncb1444
Ku70 stimulates fusion of dysfunctional telomeres yet protects chromosome ends from homologous recombination
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Abstract
Ku70–Ku80 heterodimers promote the non-homologous end-joining (NHEJ) of DNA breaks and, as shown here, the fusion of dysfunctional telomeres. Paradoxically, this heterodimer is also located at functional mammalian telomeres and interacts with components of shelterin, the protein complex that protects telomeres.
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