ArticleNature communications2026
Proteomic profiling of UV damage repair patches uncovers histone chaperones with central functions in chromatin repair.
Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed.
- July in focus in HCB: impact of environmental radiation on cells and tissues.Histochemistry and cell biology · 2026Article
- Epigenetic remodeling during UV exposure: high resolution analysis of histone post-translational modifications in a DNA binding protein 2 mutant model.Histochemistry and cell biology · 2026Article
- The interplay of DNA damage, epigenetics and tumour heterogeneity in driving cancer cell fitness.Nature communications · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
DNA damage compromises not only genome stability but also chromatin integrity, which plays a central role in controlling cell identity. Chromatin repair entails the deposition of new histones at sites of DNA damage. How this is coordinated with parental histone dynamics for the maintenance of chromatin states is unknown. To bridge this knowledge gap, here we devise a novel proteomic strategy to characterize dynamic changes in the chromatin landscape during the repair of UV-induced DNA lesions in human cells, in a quantitative, unbiased and time-resolved manner. Thus, we identify the histone chaperones DNAJC9 and MCM2 as central players in chromatin repair. DNAJC9 provides new H3-H4 histones to CAF-1 and HIRA chaperones for deposition into chromatin and stimulates old H3-H4 histone recovery. MCM2 cooperates with DNAJC9 to coordinate old and new histone dynamics during UV damage repair. Together, our proteomic dataset provides a molecular framework for further dissecting epigenome maintenance mechanisms.
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