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Replicated chromatin curtails 53BP1 recruitment in BRCA1-proficient and -deficient cells
DNA double-strand breaks can be repaired by two competing mechanisms, non-homologous end-joining (NHEJ) and homologous recombination (HR). Whether one or the other repair pathway is favored depends on the availability of an undamaged template DNA that allows for homology-directed repair. The tumor suppressor proteins 53BP1 and BRCA1 are considered antagonistic players in this repair pathway choice, as 53BP1 restrains DNA end resection, whereas BRCA1, together with its partner protein BARD1,doi:10.1101/2020.02.24.947168 fatcat:h7z3rxkxnnahnhxu7poi3wii6y