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. 2023 Jan 4;6(1):35–44. doi: 10.20517/cdr.2022.73

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© The Author(s) 2023.

© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, sharing, adaptation, distribution and reproduction in any medium or format, for any purpose, even commercially, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made.

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Effects of BOD1L/SETD1A loss on PARP inhibitor sensitivity in BRCA1-deficient cells. (A) H3K4me mediated by the BOD1L/SETD1A complex promotes RIF1 localisation at DNA double-strand breaks (DSBs) and stimulates NHEJ. In BRCA1-deficient cells, DNA-end resection and RAD51 loading are inhibited and lesions cannot be repaired by homologous recombination (HR), resulting in sensitivity to PARP inhibition and cell death. (B) Depletion of the BOD1L/SETD1A complex results in loss of H3K4me and decreased RIF1 localisation to DSBs. This allows DNA end-resection and RAD51 loading, partially restoring HR. This mediates resistance to PARP inhibition and allows cells to survive. Me: Methylation; PARP: poly(ADP) ribose polymerase; NHEJ: non-homologous end joining; KDMs: lysine demethylases.