ArticleProceedings of the National Academy of Sciences of the United States of America2013
Role of 53BP1 oligomerization in regulating double-strand break repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.
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Who cites it
56 citing papers in PubMed, 76 citations in OpenAlex.
- A Tel1-Rad9 axis links DNA double-strand break end-tethering to repair pathway choice.Nucleic acids research · 2026Article
- hTERT Increases TRF2 to Induce Telomere Compaction and Extend Cell Replicative Lifespan.Aging cell · 2025Article
- Article
- Dynamic interactions of dimeric hub proteins underlie their diverse functions and structures: A comparative analysis of 14-3-3 and LC8.The Journal of biological chemistry · 2025Review
- 53BP1 loss elicits cGAS-STING-dependent antitumor immunity in ovarian and pancreatic cancer.Nature communications · 2024Article
- ZEB1 promotes non-homologous end joining double-strand break repair.Nucleic acids research · 2023Article
- DNA-PK and the TRF2 iDDR inhibit MRN-initiated resection at leading-end telomeres.Nature structural & molecular biology · 2023Article
- SLFN5-mediated chromatin dynamics sculpt higher-order DNA repair topology.Molecular cell · 2023Article
- TRF2 rescues telomere attrition and prolongs cell survival in Duchenne muscular dystrophy cardiomyocytes derived from human iPSCs.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Review
- Multifaceted regulation and functions of 53BP1 in NHEJ‑mediated DSB repair (Review).International journal of molecular medicine · 2022Review
- 53BP1-shieldin-dependent DSB processing in BRCA1-deficient cells requires CST-Polα-primase fill-in synthesis.Nature cell biology · 2022Article
- Regulation of DNA double-strand break repair pathway choice: a new focus on 53BP1.Journal of Zhejiang University. Science. B · 2021Review
- Lysine Methyltransferase Inhibitors Impair H4K20me2 and 53BP1 Foci in Response to DNA Damage in Sarcomas, a Synthetic Lethality Strategy.Frontiers in cell and developmental biology · 2021Article
- Keeping Balance Between Genetic Stability and Plasticity at the Telomere and Subtelomere ofFrontiers in cell and developmental biology · 2021Review
- Repair of programmed DNA lesions in antibody class switch recombination: common and unique features.Genome instability & disease · 2021Review
- Spatiotemporal dynamics of 53BP1 dimer recruitment to a DNA double strand break.Nature communications · 2020Article
- DNA double-strand breaks induce H2Ax phosphorylation domains in a contact-dependent manner.Nature communications · 2020Article
- The antitumorigenic roles of BRCA1-BARD1 in DNA repair and replication.Nature reviews. Molecular cell biology · 2020Review
- 53BP1: a DSB escort.Genes & development · 2020Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Tumor suppressor p53-binding protein 1 (53BP1) regulates the repair of dysfunctional telomeres lacking the shelterin protein TRF2 by promoting their mobility, their nonhomologous end-joining (NHEJ), and, as we show here, by blocking 5' resection by CtIP. We report that these functions of 53BP1 required its N-terminal ATM/ATR target sites and its association with H4K20diMe, but not the BRCT domain, the GAR domain, or the binding of 53BP1 to dynein. A mutant lacking the oligomerization domain (53BP1(oligo)) was only modestly impaired in promoting NHEJ of dysfunctional telomeres and showed no defect with regard to the repression of CtIP. This 53BP1(oligo) allele was previously found to be unable to support class switch recombination or to promote radial chromosome formation in PARP1 inhibitor-treated Brca1-deficient cells. The data therefore support two conclusions. First, the requirements for 53BP1 in mediating NHEJ at dysfunctional telomeres and in class switch recombination are not identical. Second, 53BP1-dependent repression of CtIP at double-strand breaks (DSBs) is unlikely to be sufficient for the generation of radial chromosomes in PARP1 inhibitor-treated Brca1-deficient cells.
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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.