ReviewDNA repair2025
Base excision repair in chromatin: A tug-of-war for DNA damage.
Review in DNA repair, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 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
4 citing papers in PubMed.
- Molecular basis of nick ligation in the nucleosome by DNA Ligase IIIα.Nature communications · 2026Article
- UV-DDB as a Dynamic Regulator Linking Base Excision and Nucleotide Excision Repair via AAG Interaction.International journal of molecular sciences · 2026Article
- Facilitated DNA damage repair as an emerging therapeutic strategy for inflammatory and fibrotic diseases.RSC chemical biology · 2026Review
- Efficient and Safe Knockout ofVeterinary sciences · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
Abstract
Base excision repair (BER) is a genome surveillance pathway responsible for repairing DNA base lesions distributed throughout the chromatinized eukaryotic genome. However, chromatin structure acts as a dynamic structural barrier that restricts access to DNA and must be overcome for BER to proceed efficiently. In this perspective, we summarize recent advances that have shaped our understanding of BER in chromatin, with a focus on the structural mechanisms employed by core BER enzymes to recognize and repair DNA lesions within the nucleosome. We highlight how DNA accessibility dictates BER enzyme activity and discuss the concepts of localized and global DNA sculpting as emerging strategies for lesion recognition and repair. We propose that BER within the nucleosome represents a molecular "tug-of-war", where the histone octamer and the BER enzymes are in a constant competition for access to the damaged nucleosomal DNA. The outcome of this competition is dictated by the position of the DNA lesion within the nucleosome, which ultimately defines the efficiency of BER enzymes within chromatin. We also explore possible mechanisms used by ATP-dependent chromatin remodeling to facilitate BER within the nucleosome. Together, these recent advances provide a framework for understanding BER in chromatin and outline key unanswered questions regarding chromatin-based BER.
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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.