ArticleRadiation research2010
Deficiency in Bre1 impairs homologous recombination repair and cell cycle checkpoint response to radiation damage in mammalian cells.
Article in Radiation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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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
38 citing papers in PubMed, 58 citations in OpenAlex.
- E3 ubiquitin ligase RNF40: Structure, function and its context‑dependent roles in tumorigenesis (Review).Oncology reports · 2026Review
- Article
- RNF20 Regulates Oocyte Meiotic Spindle Assembly by Recruiting TPM3 to Centromeres and Spindle Poles.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
- The dynamics and functional mechanisms of H2B mono-ubiquitination.Crop health · 2024Review
- Bre1/RNF20 promotes Rad51-mediated strand exchange and antagonizes the Srs2/FBH1 helicases.Nature communications · 2023Article
- The Chromatin Landscape around DNA Double-Strand Breaks in Yeast and Its Influence on DNA Repair Pathway Choice.International journal of molecular sciences · 2023Review
- Chromatin Ubiquitination Guides DNA Double Strand Break Signaling and Repair.Frontiers in cell and developmental biology · 2022Review
- RNF20 affects porcine adipocyte differentiation via regulation of mitotic clonal expansion.Cell proliferation · 2021Article
- ReducedCancers · 2021Article
- RPA-mediated recruitment of Bre1 couples histone H2B ubiquitination to DNA replication and repair.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- The Role of Histone Lysine Methylation in the Response of Mammalian Cells to Ionizing Radiation.Frontiers in genetics · 2021Review
- Identification of Histone Modifications Reveals a Role of H2b Monoubiquitination in Transcriptional Regulation ofInternational journal of biological sciences · 2021Article
- Review
- Bre1-dependent H2B ubiquitination promotes homologous recombination by stimulating histone eviction at DNA breaks.Nucleic acids research · 2018Article
- DOT1L and H3K79 Methylation in Transcription and Genomic Stability.Biomolecules · 2018Review
- E3 ubiquitin ligase Bre1 couples sister chromatid cohesion establishment to DNA replication ineLife · 2017Article
- Loss of H2B monoubiquitination is associated with poor-differentiation and enhanced malignancy of lung adenocarcinoma.International journal of cancer · 2017Article
- RNF20 and histone H2B ubiquitylation exert opposing effects in Basal-Like versus luminal breast cancer.Cell death and differentiation · 2017Article
- RNF20 Links Histone H2B Ubiquitylation with Inflammation and Inflammation-Associated Cancer.Cell reports · 2016Article
- Loss of H2Bub1 Expression is Linked to Poor Prognosis in Nodal Negative Colorectal Cancers.Pathology oncology research : POR · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The pathway involving Bre1-dependent monoubiquitination of histone H2B lysine 123, which leads to Dot1-dependent methylation of histone H3 lysine 79 (H3K79me2), has been implicated in survival after exposure to ionizing radiation in Saccharomyces cerevisiae. We found that depletion of mammalian homologs of Bre1 compromises the response to ionizing radiation, leading to increased radiosensitivity and a G(2)/M checkpoint defect. The deficiency in Bre1a/b function was also associated with increased sensitivity to crosslinking drugs and defective formation of Rad51 foci in mouse cells, suggesting a defect in homologous recombinational repair analogous to that seen in Saccharomyces. In budding yeast, H3K79me2 is important for the recruitment of the checkpoint signaling protein Rad9 to sites of double-strand breaks (DSBs). However, in mammalian cells, 53BP1 (the Rad9 ortholog) in addition to H3K79me2 recognizes a different residue, H4K20me2, and some studies argue that it is H4K20me2 and not H3K79me2 that is the preferred target for 53BP1. We show here that depletion of Bre1b specifically reduced dimethylation of H3K79 without affecting dimethylation of H4K20. Thus our data suggest that the observed defects in the radiation response of Bre1a/b-deficient cells are associated with reduced H3K79me2 and not with H4K20me2.
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Registered trials
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