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Autophagy delivers damaged cytoplasmic constituents to lysosomes for degradation, thus preserving cellular integrity and protecting against disease. Remarkably, autophagy-deficient cells also exhibit aberrant DNA damage responses with therapeutic implications, such as suppression of checkpoint kinase-1 function, impaired DNA double-strand break repair by homologous recombination, and increased reliance on error-prone non-homologous end-joining for survival.
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Gillespie et al. (2015) studied this question.
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