Double-strand break end resection and repair pathway choice. Symington, L. S. & Gautier, J. Annual Review of Genetics, 45:247–271, 2011.
doi  abstract   bibtex   
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.
@article{symington_double-strand_2011,
	title = {Double-strand break end resection and repair pathway choice},
	volume = {45},
	issn = {1545-2948},
	doi = {10.1146/annurev-genet-110410-132435},
	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.},
	language = {eng},
	journal = {Annual Review of Genetics},
	author = {Symington, Lorraine S. and Gautier, Jean},
	year = {2011},
	keywords = {Animals, Cell cycle, DNA Breaks, Double-Stranded, DNA End-Joining Repair, DNA Helicases, Exodeoxyribonucleases, Fanconi Anemia, Gene Expression Regulation, Fungal, Genes, BRCA1, Genes, Fungal, Genes, cdc, Humans, Protein Conformation, Recombinational DNA Repair, Saccharomyces cerevisiae, Saccharomyces cerevisiae Proteins, Translocation, Genetic},
	pages = {247--271},
}

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