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• W3110369638 abstract "Abstract RAD52 is a member of the homologous recombination pathway that is important for survival of BRCA-deficient cells. Inhibition of RAD52 leads to lethality in BRCA-deficient cells. However, the exact mechanism of how RAD52 contributes to viability of BRCA-deficient cells remains unknown. Two major activities of RAD52 were previously identified: DNA or RNA pairing, which includes DNA/RNA annealing and strand exchange, and mediator, which is to assist RAD51 loading on RPA-covered ssDNA. Here, we report that the N-terminal domain (NTD) of RAD52 devoid of the potential mediator function is essential for maintaining viability of BRCA-deficient cells owing to its ability to promote DNA/RNA pairing. We show that RAD52 NTD forms nuclear foci upon DNA damage in BRCA-deficient human cells and promotes DNA double-strand break repair through two pathways: homology-directed repair (HDR) and single-strand annealing (SSA). Furthermore, we show that mutations in the RAD52 NTD that disrupt these activities fail to maintain viability of BRCA-deficient cells." @default.
• W3110369638 created "2020-12-07" @default.
• W3110369638 creator A5012728358 @default.
• W3110369638 creator A5071817184 @default.
• W3110369638 date "2020-12-04" @default.
• W3110369638 modified "2023-10-10" @default.
• W3110369638 title "The function of RAD52 N-terminal domain is essential for viability of BRCA-deficient cells" @default.
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• W3110369638 doi "https://doi.org/10.1093/nar/gkaa1145" @default.
• W3110369638 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/7736796" @default.
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• W3110369638 hasPublicationYear "2020" @default.
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