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Collaboration and competition between DNA double‐strand break repair pathways
Author(s) -
Kass Elizabeth M.,
Jasin Maria
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.07.057
Subject(s) - homologous recombination , dna repair , genome instability , double strand , non homologous end joining , dna , biology , microbiology and biotechnology , homology directed repair , replication protein a , dna damage , dna replication , dna repair protein xrcc4 , homologous chromosome , genetics , nucleotide excision repair , gene , dna binding protein , transcription factor
DNA double‐strand breaks resulting from normal cellular processes including replication and exogenous sources such as ionizing radiation pose a serious risk to genome stability, and cells have evolved different mechanisms for their efficient repair. The two major pathways involved in the repair of double‐strand breaks in eukaryotic cells are non‐homologous end joining and homologous recombination. Numerous factors affect the decision to repair a double‐strand break via these pathways, and accumulating evidence suggests these major repair pathways both cooperate and compete with each other at double‐strand break sites to facilitate efficient repair and promote genomic integrity.