ReviewDNA repair2015
Facilitation of base excision repair by chromatin remodeling.
Review in DNA repair, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
20 citing papers in PubMed, 32 citations in OpenAlex.
- CRISPR-mediated gap-based replacement enables site-specific DNA lesion insertion into long DNA and nucleosomes.Nucleic acids research · 2026Article
- The chromatin regulator HELLS mediates SSB repair and responses to DNA alkylation damage.Nucleic acids research · 2025Article
- Mechanisms underlying low mutation rates in mammalian oocytes and preimplantation embryos.Nucleic acids research · 2025Review
- The chromatin remodeler ERCC6 and the histone chaperone NAP1 are involved in apurinic/apyrimidinic endonuclease-mediated DNA repair.The Plant cell · 2024Article
- UV-DDB as a General Sensor of DNA Damage in Chromatin: Multifaceted Approaches to Assess Its Direct Role in Base Excision Repair.International journal of molecular sciences · 2023Review
- The Chromatin Remodeler HELLS: A New Regulator in DNA Repair, Genome Maintenance, and Cancer.International journal of molecular sciences · 2022Review
- Review
- Global and transcription-coupled repair of 8-oxoG is initiated by nucleotide excision repair proteins.Nature communications · 2022Article
- Migration speed of nucleolus precursor bodies in human male pronuclei: a novel parameter for predicting live birth.Journal of assisted reproduction and genetics · 2021Article
- Distinct roles for RSC and SWI/SNF chromatin remodelers in genomic excision repair.Genome research · 2021Article
- Virus-Host Protein-Protein Interactions between Human Papillomavirus 16 E6 A1 and D2/D3 Sub-Lineages: Variances and Similarities.International journal of molecular sciences · 2020Article
- Label-Free Proteomics Reveals the Molecular Mechanism of Subculture Induced Strain Degeneration and Discovery of Indicative Index for Degeneration inMolecules (Basel, Switzerland) · 2020Article
- Cockayne syndrome group B deficiency reduces H3K9me3 chromatin remodeler SETDB1 and exacerbates cellular aging.Nucleic acids research · 2019Article
- Damage sensor role of UV-DDB during base excision repair.Nature structural & molecular biology · 2019Article
- Stress Marks on the Genome: Use or Lose?International journal of molecular sciences · 2019Review
- Nucleosome remodelling, DNA repair and transcriptional regulation build negative feedback loops in cancer and cellular ageing.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2017Review
- Genome-wide maps of alkylation damage, repair, and mutagenesis in yeast reveal mechanisms of mutational heterogeneity.Genome research · 2017Article
- Well-positioned nucleosomes punctuate polycistronic pol II transcription units and flank silentEpigenetics & chromatin · 2017Article
- Mechanisms of Nucleosome Dynamics In Vivo.Cold Spring Harbor perspectives in medicine · 2016Review
- Nucleosomes Regulate Base Excision Repair in Chromatin.Mutation research. Reviews in mutation researchReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Base Excision Repair (BER) is a conserved, intracellular DNA repair system that recognizes and removes chemically modified bases to insure genomic integrity and prevent mutagenesis. Aberrant BER has been tightly linked with a broad spectrum of human pathologies, such as several types of cancer, neurological degeneration, developmental abnormalities, immune dysfunction and aging. In the cell, BER must recognize and remove DNA lesions from the tightly condensed, protein-coated chromatin. Because chromatin is necessarily refractory to DNA metabolic processes, like transcription and replication, the compaction of the genomic material is also inhibitory to the repair systems necessary for its upkeep. Multiple ATP-dependent chromatin remodelling (ACR) complexes play essential roles in modulating the protein-DNA interactions within chromatin, regulating transcription and promoting activities of some DNA repair systems, including double-strand break repair and nucleotide excision repair. However, it remains unclear how BER operates in the context of chromatin, and if the chromatin remodelling processes that govern transcription and replication also actively regulate the efficiency of BER. In this review we highlight the emerging role of ACR in regulation of BER.
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What OpenQuestion holds
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.