ArticleNature communications2024
Widespread chromatin context-dependencies of DNA double-strand break repair proteins.
Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Activation of Pol theta-mediated end joining begins during mitotic commitment.bioRxiv : the preprint server for biology · 2026Article
- Origins and consequences of oncogenic 3D chromatin remodelling.Nature reviews. Cancer · 2026Review
- Using the DNA language model, GROVER, to parse effects of sequence, chromatin and regulatory features on genome stability.Bioinformatics (Oxford, England) · 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
- iMUT-seq mapping of DSB-induced mutations with high sensitivity at single-nucleotide resolution.Nature protocols · 2026Review
- CRISPR/Cas9-Based Genome Editing: Understanding Differences in DNA Repair Pathways, Profiles, and Outcomes.International journal of molecular sciences · 2026Review
- Indel pattern-guided repair mapping reveals genome-wide DNA repair networks in CRISPR/Cas9 editing.Nucleic acids research · 2026Article
- Dual-single-guide RNA strategy improves CRISPR-mediated homology-directed repair in Aspergillus.Nucleic acids research · 2026Article
- PARP1 and PARP2 are dispensable for DNA repair by microhomology-mediated end-joining at double-ended DSBs.Nucleic acids research · 2026Article
- A base editing resource for functional annotation of DNA repair variants in breast-derived cell models.Frontiers in cell and developmental biology · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- From survival of irradiated mice to modern molecular insights: a seventy-year journey in radiobiology at the institute of biophysics, Czech academy of sciences.European biophysics journal : EBJ · 2025Review
- Review
- Review
- FOXD3 promotes homologous recombination repair and genomic stability by facilitating MRE11-mediated DNA end resection.Acta biochimica et biophysica Sinica · 2025Article
- CDK1 mediates the metabolic regulation of DNA double-strand break repair in metaphase II oocytes.BMC biology · 2025Article
- DNA double-strand break movement in heterochromatin depends on the histone acetyltransferase dGcn5.Nucleic acids research · 2024Article
- Chromatin context-dependent effects of epigenetic drugs on CRISPR-Cas9 editing.Nucleic acids research · 2024Article
- Widespread chromatin context-dependencies of DNA double-strand break repair proteins.Nature communications · 2024Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors.
Funding
Abstract
DNA double-strand breaks are repaired by multiple pathways, including non-homologous end-joining (NHEJ) and microhomology-mediated end-joining (MMEJ). The balance of these pathways is dependent on the local chromatin context, but the underlying mechanisms are poorly understood. By combining knockout screening with a dual MMEJ:NHEJ reporter inserted in 19 different chromatin environments, we identified dozens of DNA repair proteins that modulate pathway balance dependent on the local chromatin state. Proteins that favor NHEJ mostly synergize with euchromatin, while proteins that favor MMEJ generally synergize with distinct types of heterochromatin. Examples of the former are BRCA2 and POLL, and of the latter the FANC complex and ATM. Moreover, in a diversity of human cancer types, loss of several of these proteins alters the distribution of pathway-specific mutations between heterochromatin and euchromatin. Together, these results uncover a complex network of proteins that regulate MMEJ:NHEJ balance in a chromatin context-dependent manner.
Indexed as
Identifiers
What Socratic 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 Socratic graph.