ArticleNature2013
53BP1 is a reader of the DNA-damage-induced H2A Lys 15 ubiquitin mark.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 443 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
443 citing papers in PubMed, 676 citations in OpenAlex.
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- Histone modifications: mechanisms, metabolic regulation, and therapeutic targeting in cancer.Precision clinical medicine · 2026Review
- RSF1-Dependent PAR Turnover Promotes 53BP1 Liquid Condensate Formation at DNA Damage Sites.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- A ubiquitin chain-feeding mechanism for BRCA1-A.Nature communications · 2026Article
- CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks.Nucleic acids research · 2026Article
- Eukaryotic translation elongation factor 1 delta alleviates DNA damage during bovine alphaherpesvirus 1 infection.Journal of veterinary science · 2026Article
- Dual roles of the DHX9 RGG domain in hybrid-dependent recruitment and suppression of 53BP1.Scientific reports · 2026Article
- DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer.Cancer research · 2026Article
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- Chromatin Remodeling, DNA Double-Strand Break Repair, and Human Disease: How a Breakup Changes You.Biomolecules · 2026Review
- Time-dependent 53BP1 foci kinetics in X-irradiated human hair follicle dermal papilla cells.Journal of radiation research · 2026Article
- Article
- Mono-ubiquitination of histone H2A lysine 119 (H2AK119Ub): its multifaceted role in biology and implication in diseases.MedScience · 2026Review
- Circadian regulation of homologous recombination by cryptochrome1-mediated dampening of DNA end resection.Nature communications · 2025Article
- Synergistic antitumor and radiosensitizing effects of α-sulfoquinovosyl-acylpropanediol (SQAP) via PI3K/Akt inhibition and DNA repair impairment in glioblastoma.Journal of neuro-oncology · 2025Article
- How histone modifications influence cellular radiosensitivity: Pharmaceutically targeting epigenetic regulators as a promising avenue to overcome radioresistance.Acta pharmaceutica Sinica. B · 2025Review
- GSK3B directs DNA repair choice and determines tumor response to PARP1 inhibition independent of BRCA1.The Journal of clinical investigation · 2025Article
- Specific TP53 mutations impair the recruitment of 53BP1 to DNA double-strand breaks underlying the mechanism of radioresistance.European biophysics journal : EBJ · 2025Article
383 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern
Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
53BP1 (also called TP53BP1) is a chromatin-associated factor that promotes immunoglobulin class switching and DNA double-strand-break (DSB) repair by non-homologous end joining. To accomplish its function in DNA repair, 53BP1 accumulates at DSB sites downstream of the RNF168 ubiquitin ligase. How ubiquitin recruits 53BP1 to break sites remains unknown as its relocalization involves recognition of histone H4 Lys 20 (H4K20) methylation by its Tudor domain. Here we elucidate how vertebrate 53BP1 is recruited to the chromatin that flanks DSB sites. We show that 53BP1 recognizes mononucleosomes containing dimethylated H4K20 (H4K20me2) and H2A ubiquitinated on Lys 15 (H2AK15ub), the latter being a product of RNF168 action on chromatin. 53BP1 binds to nucleosomes minimally as a dimer using its previously characterized methyl-lysine-binding Tudor domain and a carboxy-terminal extension, termed the ubiquitination-dependent recruitment (UDR) motif, which interacts with the epitope formed by H2AK15ub and its surrounding residues on the H2A tail. 53BP1 is therefore a bivalent histone modification reader that recognizes a histone 'code' produced by DSB signalling.
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What OpenQuestion holds
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.