ArticleNature chemical biology2015
Chemical proteomics reveals a γH2AX-53BP1 interaction in the DNA damage response.
Article in Nature chemical biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.
What it found
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Who cites it
68 citing papers in PubMed, 107 citations in OpenAlex.
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- Autoimmune neuroinflammation leads to neuronal death via MIF nuclease-mediated parthanatos.Nature neuroscience · 2026Article
- Histone probes for reader and eraser investigations.Chemical science · 2025Review
- Small Extracellular Vesicles From Radioresistant H3K27M-Pediatric Diffuse Midline Glioma Cells Modulate Tumor Phenotypes and Radiation Response.Journal of extracellular vesicles · 2025Article
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- Carbon ion irradiation conquers the radioresistance by inducing complex DNA damage and apoptosis in U251 human glioblastomas cells.Medical oncology (Northwood, London, England) · 2025Article
- Global γH2AX phosphorylation inmicroPublication biology · 2025Article
- DPF2 reads histone lactylation to drive transcription and tumorigenesis.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- ATR inhibition radiosensitizes cells through augmented DNA damage and G2 cell cycle arrest abrogation.JCI insight · 2024Article
- Phosphorylation of the DNA damage repair factor 53BP1 by ATM kinase controls neurodevelopmental programs in cortical brain organoids.PLoS biology · 2024Article
- Evolved histone tail regulates 53BP1 recruitment at damaged chromatin.Nature communications · 2024Article
- H2AX promotes replication fork degradation and chemosensitivity in BRCA-deficient tumours.Nature communications · 2024Article
- Interrogating epigenetic mechanisms with chemically customized chromatin.Nature reviews. Genetics · 2024Review
- Trypanosoma cruzi infection induces DNA double-strand breaks and activates DNA damage response pathway in host epithelial cells.Scientific reports · 2024Article
- Impaired end joining induces cardiac atrophy in a Hutchinson-Gilford progeria mouse model.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Article
- Pectolinarigenin inhibits bladder urothelial carcinoma cell proliferation by regulating DNA damage/autophagy pathways.Cell death discovery · 2023Article
- High-throughput measurement of double strand break global repair phenotype in peripheral blood mononuclear cells after long-term cryopreservation.Cytometry. Part A : the journal of the International Society for Analytical Cytology · 2023Article
- Histone variant-specific post-translational modifications.Seminars in cell & developmental biology · 2023Review
- Histone H2A variants: Diversifying chromatin to ensure genome integrity.Seminars in cell & developmental biology · 2023Review
8 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
DNA double-strand break repair involves phosphorylation of histone variant H2AX ('γH2AX'), which accumulates in foci at sites of DNA damage. In current models, the recruitment of multiple DNA repair proteins to γH2AX foci depends mainly on recognition of this 'mark' by a single protein, MDC1. However, DNA repair proteins accumulate at γH2AX sites without MDC1, suggesting that other 'readers' of this mark exist. Here, we use a quantitative chemical proteomics approach to profile direct, phospho-selective γH2AX binders in native proteomes. We identify γH2AX binders, including the DNA repair mediator 53BP1, which we show recognizes γH2AX through its BRCT domains. Furthermore, we investigate the targeting of wild-type 53BP1, or a mutant form deficient in γH2AX binding, to chromosomal breaks resulting from endogenous and exogenous DNA damage. Our results show how direct recognition of γH2AX modulates protein localization at DNA damage sites, and suggest how specific chromatin mark-reader interactions contribute to essential mechanisms ensuring genome stability.
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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.