ReviewBiomolecules2016
Repair of DNA Double-Strand Breaks in Heterochromatin.
Review in Biomolecules, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed.
- CHAMP1 complex directs heterochromatin assembly and promotes homology-directed DNA repair.Nature communications · 2025Article
- Heterochromatin repeat organization at an individual level: Rex1BD and the 14-3-3 protein coordinate to shape the epigenetic landscape within heterochromatin repeats.BioEssays : news and reviews in molecular, cellular and developmental biology · 2024Review
- Rex1BD and the 14-3-3 protein control heterochromatin organization at tandem repeats by linking RNAi and HDAC.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- High-LET-Radiation-Induced Persistent DNA Damage Response Signaling and Gastrointestinal Cancer Development.Current oncology (Toronto, Ont.) · 2023Review
- Genome-wide identification of copy neutral loss of heterozygosity reveals its possible association with spatial positioning of chromosomes.Human molecular genetics · 2023Article
- Purifying selection on noncoding deletions of human regulatory loci detected using their cellular pleiotropy.Genome research · 2021Article
- Molecular Aspects of Senescence and Organismal Ageing-DNA Damage Response, Telomeres, Inflammation and Chromatin.International journal of molecular sciences · 2021Review
- Review
- Systematic analysis of linker histone PTM hotspots reveals phosphorylation sites that modulate homologous recombination and DSB repair.DNA repair · 2020Article
- Article
- The Chromatin Structure of CRISPR-Cas9 Target DNA Controls the Balance between Mutagenic and Homology-Directed Gene-Editing Events.Molecular therapy. Nucleic acids · 2019Article
- Cellular responses to ionizing radiation change quickly over time during early development in zebrafish.Cell biology international · 2019Article
- CHD4 regulates the DNA damage response and RAD51 expression in glioblastoma.Scientific reports · 2019Article
- Efficient Homologous Recombination in Mice Using Long Single Stranded DNA and CRISPR Cas9 Nickase.G3 (Bethesda, Md.) · 2019Article
- Moving Mountains-The BRCA1 Promotion of DNA Resection.Frontiers in molecular biosciences · 2019Review
- Fast calculation of nanodosimetric quantities in treatment planning of proton and ion therapy.Physics in medicine and biology · 2018Article
- Article
- Heterochromatin and DNA damage repair: Use different histone variants and relax.Nucleus (Austin, Tex.) · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author.
Funding
Abstract
DNA double-strand breaks (DSBs) are among the most damaging lesions in DNA, since, if not identified and repaired, they can lead to insertions, deletions or chromosomal rearrangements. DSBs can be in the form of simple or complex breaks, and may be repaired by one of a number of processes, the nature of which depends on the complexity of the break or the position of the break within the chromatin. In eukaryotic cells, nuclear DNA is maintained as either euchromatin (EC) which is loosely packed, or in a denser form, much of which is heterochromatin (HC). Due to the less accessible nature of the DNA in HC as compared to that in EC, repair of damage in HC is not as straightforward as repair in EC. Here we review the literature on how cells deal with DSBs in HC.
Indexed as
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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.