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Article

Distinct roles of RAD52 and POLQ in chromosomal break repair and replication stress response

5 Aug 2019

Abstract excerpt

Disrupting either the DNA annealing factor RAD52 or the A-family DNA polymerase POLQ can cause synthetic lethality with defects in BRCA1 and BRCA2, which are tumor suppressors important for homology-directed repair of DNA double-strand breaks (DSBs), and protection of stalled replication forks. A likely mechanism of this synthetic lethality is that RAD52 and/or POLQ are important for backup pathways for DSB...

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Identifiers

PMID: 31381562
DOI: 10.1371/journal.pgen.1008319

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