ArticleCell cycle (Georgetown, Tex.)2015
Ubiquitin-H2AX fusions render 53BP1 recruitment to DNA damage sites independent of RNF8 or RNF168.
Article in Cell cycle (Georgetown, Tex.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Structural insights into γH2Ax containing nucleosomes.Nucleic acids research · 2025Article
- PIN1-SUMO2/3 motif suppresses excessive RNF168 chromatin accumulation and ubiquitin signaling to promote IR resistance.Nature communications · 2025Article
- Histone Phosphorylation in DNA Damage Response.International journal of molecular sciences · 2025Review
- ZEB1 promotes DNA homologous recombination repair and contributes to the 5-Fluorouracil resistance in colorectal cancer.American journal of cancer research · 2023Article
- Fast friends - Ubiquitin-like modifiers as engineered fusion partners.Seminars in cell & developmental biology · 2022Review
- RNF168-Mediated Ubiquitin Signaling Inhibits the Viability ofCancer research · 2020Article
- Ectopic RNF168 expression promotes break-induced replication-like DNA synthesis at stalled replication forks.Nucleic acids research · 2020Article
- A bi-terminal protein ligation strategy to probe chromatin structure during DNA damage.Chemical science · 2018Article
- Epigenomic Modifications Mediating Antibody Maturation.Frontiers in immunology · 2018Review
- Reading chromatin signatures after DNA double-strand breaks.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Article
- Chronic oxidative stress promotes H2AX protein degradation and enhances chemosensitivity in breast cancer patients.EMBO molecular medicine · 2016Article
- Choreographing the Double Strand Break Response: Ubiquitin and SUMO Control of Nuclear Architecture.Frontiers in genetics · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The mammalian E3 ubiquitin ligases RNF8 and RNF168 facilitate recruitment of the DNA damage response protein 53BP1 to sites of DNA double-strand breaks (DSBs). The mechanism involves recruitment of RNF8, followed by recruitment of RNF168, which ubiquitinates histones H2A/H2AX on K15. 53BP1 then binds to nucleosomes at sites of DNA DSBs by recognizing, in addition to methyl marks, histone H2A/H2AX ubiquitinated on K15. We report here that expressing H2AX fusion proteins with N-terminal bulky moieties can rescue 53BP1 recruitment to sites of DNA DSBs in cells lacking RNF8 or RNF168 or in cells treated with proteasome inhibitors, in which histone ubiquitination at sites of DNA DSBs is compromised. The rescue required S139 at the C-terminus of the H2AX fusion protein and was occasionally accompanied by partial rescue of ubiquitination at sites of DNA DSBs. We conclude that recruitment of 53BP1 to sites of DNA DSBs is possible in the absence of RNF8 or RNF168, but still dependent on chromatin ubiquitination.
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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.