期刊
ANNUAL REVIEW OF GENETICS, VOL 45
卷 45, 期 -, 页码 247-271出版社
ANNUAL REVIEWS
DOI: 10.1146/annurev-genet-110410-132435
关键词
homologous recombination; MRX/N; Sae2/CtIP/Ctp1; Ku; checkpoint; nonhomologous end joining
资金
- NCI NIH HHS [CA092245] Funding Source: Medline
- NIGMS NIH HHS [GM077496, R01 GM041784-22, R01 GM041784, GM094386, R01 GM041784-23, GM041784] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA092245] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM094386, R01GM041784] Funding Source: NIH RePORTER
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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