ArticleNature structural & molecular biology2014
Transcriptionally active chromatin recruits homologous recombination at DNA double-strand breaks.
Article in Nature structural & molecular biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 427 papers, 1 of them a synthesis that pooled it.
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.
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Who cites it
427 citing papers in PubMed, 1 synthesis or guideline pooled it, 661 citations in OpenAlex.
- DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci.Nucleic acids research · 2022Pooled it
- The nuclear pore complex as a spatial organizing hub for high-risk DNA lesions.Nucleus (Austin, Tex.) · 2026Review
- Persistent TOP1 cleavage complexes in drug-tolerant cells drive adaptive resistance to EGFR-targeted therapies in lung cancer.Science advances · 2026Article
- DDX3X regulates DNA repair pathway choice at double-strand breaks via RNA-DNA hybrid formation.Cell death and differentiation · 2026Article
- Targeting the DNA-repair chromatin-modifier protein SMYD3 as a novel epigenetics-based therapy for gastric cancer.Journal of experimental & clinical cancer research : CR · 2026Article
- Suppression of transcription-replication conflicts by sequence-coordinated actions of TRDMT1 and MutLα.Nature communications · 2026Article
- HELZ is a RNA-DNA helicase that resolves R loops to facilitate homologous recombination repair.Nature communications · 2026Article
- CTCF primes repressive chromatin for rapid BRCA1/BARD1 recruitment to drive homologous recombination repair of DNA double-strand breaks.Nucleic acids research · 2026Article
- iMUT-seq mapping of DSB-induced mutations with high sensitivity at single-nucleotide resolution.Nature protocols · 2026Review
- R-loops and D-loops: a delicate balance in genomic stability and instability.Cell communication and signaling : CCS · 2026Review
- DPY30 Is an Epigenetic Decoupler Linking Replication Stress to Immunoediting in Pancreatic Cancer.Cancer research · 2026Article
- ID3 deficiency alters chromatin accessibility at DSB sites and enhances vulnerability to HDAC inhibition.International journal of cancer · 2026Article
- Toward a Conceptual Multiscale Framework for Predictive Radiobiology: Integrating Genomic Damage, Network Rewiring, and Tissue Microenvironment.International journal of molecular sciences · 2026Review
- G quadruplex DNA facilitates a pervasive path to homologous recombination.bioRxiv : the preprint server for biology · 2026Article
- cGAS restricts PARP1-mediated microhomology-mediated end joining by suppressing poly-ADP-ribosylation.Cell death and differentiation · 2026Article
- Centromeric α-satellite DNA is a hotspot of genotoxic damage, incomplete repair, and cytoplasmic mislocalization.bioRxiv : the preprint server for biology · 2026Article
- SFPQ Promotes Homologous Recombination via mRNA Stabilization of RAD51 and Its Paralogs.Journal of molecular biology · 2026Article
- TTNPB Promotes Human Pluripotent Stem Cell-to-Neural Stem Cell Transition via Modulation of Chromatin Accessibility and the S-(5'-adenosyl)-L-homocysteine/Choline Metabolic Network.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Features affecting Cas9-induced editing efficiency and patterns in tomato: evidence from a large CRISPR dataset.The Plant journal : for cell and molecular biology · 2026Article
- Article
367 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 5 institutions in 2 countries.
Funding
Abstract
Although both homologous recombination (HR) and nonhomologous end joining can repair DNA double-strand breaks (DSBs), the mechanisms by which one of these pathways is chosen over the other remain unclear. Here we show that transcriptionally active chromatin is preferentially repaired by HR. Using chromatin immunoprecipitation-sequencing (ChIP-seq) to analyze repair of multiple DSBs induced throughout the human genome, we identify an HR-prone subset of DSBs that recruit the HR protein RAD51, undergo resection and rely on RAD51 for efficient repair. These DSBs are located in actively transcribed genes and are targeted to HR repair via the transcription elongation-associated mark trimethylated histone H3 K36. Concordantly, depletion of SETD2, the main H3 K36 trimethyltransferase, severely impedes HR at such DSBs. Our study thereby demonstrates a primary role in DSB repair of the chromatin context in which a break occurs.
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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.