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- W4280491403 abstract "DNA double-strand break (DSB) repair by homologous recombination is confined to the S and G2 phases of the cell cycle partly due to 53BP1 antagonizing DNA end resection in G1 phase and non-cycling quiescent (G0) cells where DSBs are predominately repaired by non-homologous end joining (NHEJ). Unexpectedly, we uncovered extensive MRE11- and CtIP-dependent DNA end resection at DSBs in G0 murine and human cells. A whole genome CRISPR/Cas9 screen revealed the DNA-dependent kinase (DNA-PK) complex as a key factor in promoting DNA end resection in G0 cells. In agreement, depletion of FBXL12, which promotes ubiquitylation and removal of the KU70/KU80 subunits of DNA-PK from DSBs, promotes even more extensive resection in G0 cells. In contrast, a requirement for DNA-PK in promoting DNA end resection in proliferating cells at the G1 or G2 phase of the cell cycle was not observed. Our findings establish that DNA-PK uniquely promotes DNA end resection in G0, but not in G1 or G2 phase cells, which has important implications for DNA DSB repair in quiescent cells." @default.
- W4280491403 created "2022-05-22" @default.
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- W4280491403 date "2022-05-16" @default.
- W4280491403 modified "2023-10-14" @default.
- W4280491403 title "DNA-PK promotes DNA end resection at DNA double strand breaks in G0 cells" @default.
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- W4280491403 doi "https://doi.org/10.7554/elife.74700" @default.
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- W4280491403 hasPublicationYear "2022" @default.
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