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      Double-strand break end resection and repair pathway choice.

      Annual review of genetics

      Translocation, Genetic, genetics, chemistry, Saccharomyces cerevisiae Proteins, Saccharomyces cerevisiae, Recombinational DNA Repair, Protein Conformation, Humans, Genes, cdc, Genes, Fungal, Genes, BRCA1, Gene Expression Regulation, Fungal, Fanconi Anemia, Exodeoxyribonucleases, DNA Helicases, DNA End-Joining Repair, DNA Breaks, Double-Stranded, Cell Cycle, Animals

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          Abstract

          DNA double-strand breaks (DSBs) are cytotoxic lesions that can result in mutagenic events or cell death if left unrepaired or repaired inappropriately. Cells use two major pathways for DSB repair: nonhomologous end joining (NHEJ) and homologous recombination (HR). The choice between these pathways depends on the phase of the cell cycle and the nature of the DSB ends. A critical determinant of repair pathway choice is the initiation of 5'-3' resection of DNA ends, which commits cells to homology-dependent repair, and prevents repair by classical NHEJ. Here, we review the components of the end resection machinery, the role of end structure, and the cell-cycle phase on resection and the interplay of end processing with NHEJ.

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          Author and article information

          Journal
          21910633
          10.1146/annurev-genet-110410-132435

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