ArticleScientific reports2017
Spatially restricted loading of BRD2 at DNA double-strand breaks protects H4 acetylation domains and promotes DNA repair.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Maternal dysglycaemia, changes in the infant's epigenome modified with a diet and physical activity intervention in pregnancy: Secondary analysis of a randomised control trial.PLoS medicine · 2020Trial
- Identification of BET inhibitors (BETi) against solitary fibrous tumor (SFT) through high-throughput screening (HTS).Neoplasia (New York, N.Y.) · 2025Article
- Histone Modifications in the Anoxic Northern Crayfish, Faxonius virilis.Marine biotechnology (New York, N.Y.) · 2024Article
- BRD2 promotes antibody class switch recombination by facilitating DNA repair in collaboration with NIPBL.Nucleic acids research · 2024Article
- The consequences of viral infection on host DNA damage response: a focus on SARS-CoVs.Journal, genetic engineering & biotechnology · 2022Review
- Precision Medicine forCancers · 2022Review
- The Chromatin Landscape Channels DNA Double-Strand Breaks to Distinct Repair Pathways.Frontiers in cell and developmental biology · 2022Review
- CopyCatchers are versatile active genetic elements that detect and quantify inter-homolog somatic gene conversion.Nature communications · 2021Article
- Regulation of ZMYND8 to Treat Cancer.Molecules (Basel, Switzerland) · 2021Review
- Oocyte Meiotic Competence in the Domestic Cat Model: Novel Roles for Nuclear Proteins BRD2 and NPM1.Frontiers in cell and developmental biology · 2021Article
- Article
- The Functions of BET Proteins in Gene Transcription of Biology and Diseases.Frontiers in molecular biosciences · 2021Review
- Identification of candidate genetic variants and altered protein expression in neural stem and mature neural cells support altered microtubule function to be an essential component in bipolar disorder.Translational psychiatry · 2020Article
- Review
- 53BP1/RIF1 signaling promotes cell survival after multifractionated radiotherapy.Nucleic acids research · 2020Article
- PHF6 promotes non-homologous end joining and G2 checkpoint recovery.EMBO reports · 2020Article
- Functional Analysis of the Replication Fork Proteome Identifies BET Proteins as PCNA Regulators.Cell reports · 2019Article
- The function of histone acetylation in cervical cancer development.Bioscience reports · 2019Review
- Multiple Roles for Mono- and Poly(ADP-Ribose) in Regulating Stress Responses.Trends in genetics : TIG · 2019Review
- Moving Mountains-The BRCA1 Promotion of DNA Resection.Frontiers in molecular biosciences · 2019Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The n-terminal tail of histone H4 recruits repair proteins, including 53BP1, to DNA double-strand breaks (DSB) and undergoes dynamic acetylation during DSB repair. However, how H4 acetylation (H4Ac) recruits repair proteins and reorganizes chromatin during DNA repair is unclear. Here, we show that the bromodomain protein BRD2 is recruited to DSBs. This recruitment requires binding of BRD2's tandem bromodomains to H4Ac, which is generated at DSBs by the Tip60/KAT5 acetyltransferase. Binding of BRD2 to H4Ac protects the underlying acetylated chromatin from attack by histone deacetylases and allows acetylation to spread along the flanking chromatin. However, BRD2 recruitment is spatially restricted to a chromatin domain extending only 2 kb either side of the DSB, and BRD2 does not spread into the chromatin domains flanking the break. Instead, BRD2 facilitates recruitment of a second bromodomain protein, ZMYND8, which spreads along the flanking chromatin, but is excluded from the DSB region. This creates a spatially restricted H4Ac/BRD2 domain which reorganizes chromatin at DSBs, limits binding of the L3MBTL1 repressor and promotes 53BP1 binding, while limiting end-resection of DSBs. BRD2 therefore creates a restricted chromatin environment surrounding DSBs which facilitates DSB repair and which is framed by extensive ZMYND8 domains on the flanking chromatin.
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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.