ArticleNature structural & molecular biology2016
53BP1 fosters fidelity of homology-directed DNA repair.
Article in Nature structural & molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 153 papers.
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Who cites it
153 citing papers in PubMed, 222 citations in OpenAlex.
- The dynamics of RAD51 foci formation and elongation in living human cells.Nucleic acids research · 2026Article
- A Tel1-Rad9 axis links DNA double-strand break end-tethering to repair pathway choice.Nucleic acids research · 2026Article
- CDW19S coordinates phasic end processing via distinct enzymatic activities.Nucleic acids research · 2026Article
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- Base-excision repair increases DNA double-strand break clustering within heavy-ion tracks and modulates repair at δ-electron-induced breaks.Scientific reports · 2026Article
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Imaging the time course of DNA damage response at a nonrepetitive endogenous locus.Cell reports methods · 2025Article
- Review
- Research Advances of the Autophagy-Regulated Radiosensitivity.Cell proliferation · 2025Review
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- p53-deficient cancer cells hyperactivate DNA double-strand break repair pathways to overcome chemotherapeutic damage and augment survival.Molecular biology reports · 2025Article
- Interplay and Dynamics of Chromatin Architecture and DNA Damage Response: An Overview.Cancers · 2025Review
- Homologous recombination promotes non-immunogenic mitotic cell death upon DNA damage.Nature cell biology · 2025Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).Nature communications · 2024Article
- NEAT1 modulates the TIRR/53BP1 complex to maintain genome integrity.Nature communications · 2024Article
- 53BP1 deficiency leads to hyperrecombination using break-induced replication (BIR).bioRxiv : the preprint server for biology · 2024Article
- Cyclin F-EXO1 axis controls cell cycle-dependent execution of double-strand break repair.Science advances · 2024Article
- Article
- EXO1 protects BRCA1-deficient cells against toxic DNA lesions.Molecular cell · 2024Article
93 more citing papers are in PubMed but not listed here.
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Repair of DNA double-strand breaks (DSBs) in mammals is coordinated by the ubiquitin-dependent accumulation of 53BP1 at DSB-flanking chromatin. Owing to its ability to limit DNA-end processing, 53BP1 is thought to promote nonhomologous end-joining (NHEJ) and to suppress homology-directed repair (HDR). Here, we show that silencing 53BP1 or exhausting its capacity to bind damaged chromatin changes limited DSB resection to hyper-resection and results in a switch from error-free gene conversion by RAD51 to mutagenic single-strand annealing by RAD52. Thus, rather than suppressing HDR, 53BP1 fosters its fidelity. These findings illuminate causes and consequences of synthetic viability acquired through 53BP1 silencing in cells lacking the BRCA1 tumor suppressor. We show that such cells survive DSB assaults at the cost of increasing reliance on RAD52-mediated HDR, which may fuel genome instability. However, our findings suggest that when challenged by DSBs, BRCA1- and 53BP1-deficient cells may become hypersensitive to, and be eliminated by, RAD52 inhibition.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.