ReviewJournal of molecular biology2016
Patching Broken DNA: Nucleosome Dynamics and the Repair of DNA Breaks.
Review in Journal of molecular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
70 citing papers in PubMed, 109 citations in OpenAlex.
- Article
- H2A.Z-nucleosomes are stabilized by the superhelicity-dependent DNA binding of the C-terminal tail of the histone variant.Nucleus (Austin, Tex.) · 2025Article
- High Molecular Crowding in Repair Foci Surrounding DNA Breaks, Measured by Fluorescence Lifetime Imaging Microscopy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Histone acetylation readers Bdf1 and Yaf9 direct SWR1 remodeler to +1 nucleosome.Science advances · 2025Article
- Cryo-EM structures reveal the acetylation process of piccolo NuA4.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- The translatome of glioblastoma.Molecular oncology · 2025Article
- The "Ins and Outs and What-Abouts" of H2A.Z: A tribute to C. David Allis.The Journal of biological chemistry · 2025Article
- Multifunctional histone variants in genome function.Nature reviews. Genetics · 2025Review
- ATAD5-BAZ1B interaction modulates PCNA ubiquitination during DNA repair.Nature communications · 2024Article
- Stabilization of the hexasome intermediate during histone exchange by yeast SWR1 complex.Molecular cell · 2024Article
- Synergistic Cytotoxicity of Histone Deacetylase and Poly-ADP Ribose Polymerase Inhibitors and Decitabine in Breast and Ovarian Cancer Cells: Implications for Novel Therapeutic Combinations.International journal of molecular sciences · 2024Article
- Article
- DNA damage and repair in the nucleosome: insights from computational methods.Biophysical reviews · 2024Review
- The molecular details of a novel phosphorylation-dependent interaction between MRN and the SOSS complex.Protein science : a publication of the Protein Society · 2023Article
- Zinc finger transcription factor CASZ1b is involved in the DNA damage response in live cells.Biochemical and biophysical research communications · 2023Article
- DNA double-strand break end synapsis by DNA loop extrusion.Nature communications · 2023Article
- Synergistic cytotoxicity of fludarabine, clofarabine, busulfan, vorinostat and olaparib in AML cells.Frontiers in oncology · 2023Article
- Chromatin accessibility: methods, mechanisms, and biological insights.Nucleus (Austin, Tex.) · 2022Review
- Article
- Functional mapping of PHF6 complexes in chromatin remodeling, replication dynamics, and DNA repair.Blood · 2022Article
10 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The ability of cells to detect and repair DNA double-strand breaks (DSBs) is dependent on reorganization of the surrounding chromatin structure by chromatin remodeling complexes. These complexes promote access to the site of DNA damage, facilitate processing of the damaged DNA and, importantly, are essential to repackage the repaired DNA. Here, we will review the chromatin remodeling steps that occur immediately after DSB production and that prepare the damaged chromatin template for processing by the DSB repair machinery. DSBs promote rapid accumulation of repressive complexes, including HP1, the NuRD complex, H2A.Z and histone methyltransferases at the DSB. This shift to a repressive chromatin organization may be important to inhibit local transcription and limit mobility of the break and to maintain the DNA ends in close contact. Subsequently, the repressive chromatin is rapidly dismantled through a mechanism involving dynamic exchange of the histone variant H2A.Z. H2A.Z removal at DSBs alters the acidic patch on the nucleosome surface, promoting acetylation of the H4 tail (by the NuA4-Tip60 complex) and shifting the chromatin to a more open structure. Further, H2A.Z removal promotes chromatin ubiquitination and recruitment of additional DSB repair proteins to the break. Modulation of the nucleosome surface and nucleosome function during DSB repair therefore plays a vital role in processing of DNA breaks. Further, the nucleosome surface may function as a central hub during DSB repair, directing specific patterns of histone modification, recruiting DNA repair proteins and modulating chromatin packing during processing of the damaged DNA template.
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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.