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Letter
Nature Genetics 37, 193–197 (1 February 2005) | doi:10.1038/ng1506
Human telomeric protein TRF2 associates with genomic double-strand breaks as an early response to DNA damage
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Abstract
DNA damage surveillance networks in human cells can activate DNA repair, cell cycle checkpoints and apoptosis in response to fewer than four double-strand breaks (DSBs) per genome. These same networks tolerate telomeres, in part because the protein TRF2 prevents recognition of telomeric ends as DSBs by facilitating their organization into T loops.
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