53BP1 cooperation with the REV7-shieldin complex underpins DNA structure-specific NHEJ.

ABSTRACT: 53BP1 governs a specialized, context-specific branch of the classical non-homologous end joining DNA double-strand break repair pathway. Mice lacking 53bp1 (also known as Trp53bp1) are immunodeficient owing to a complete loss of immunoglobulin class-switch recombination^1,2, and reduced fidelity of long-range V(D)J recombination³. The 53BP1-dependent pathway is also responsible for pathological joining events at dysfunctional telomeres⁴, and its unrestricted activity in Brca1-deficient cellular and tumour models causes genomic instability and oncogenesis^5-7. Cells that lack core non-homologous end joining proteins are profoundly radiosensitive⁸, unlike 53BP1-deficient cells^9,10, which suggests that 53BP1 and its co-factors ac

SUBMITTER: Ghezraoui H 

PROVIDER: S-EPMC6989217 | biostudies-literature | 2018 Aug

REPOSITORIES: biostudies-literature