ArticleProceedings of the National Academy of Sciences of the United States of America2014
Homology-directed repair of DNA nicks via pathways distinct from canonical double-strand break repair.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 128 papers, 1 of them a synthesis that pooled it.
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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.
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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
128 citing papers in PubMed, 1 synthesis or guideline pooled it, 203 citations in OpenAlex.
- Rare variants in BRCA2 and CHEK2 are associated with the risk of urinary tract cancers.Scientific reports · 2016Pooled it
- DNA damage induces long range changes to duplex structure-a non-protein start to damage detection?Nucleic acids research · 2026Article
- 53BP1-independent Shieldin-BRCA1 antagonism at replication-coupled double-strand breaks.Nature communications · 2026Article
- Application and Research Prospects of CRISPR/Cas Gene Editing Technology in Lactic Acid Bacteria.Microorganisms · 2026Review
- SETDB1/ATF7IP regulate the precise genome engineering of HUSH-regulated genes.Epigenetics & chromatin · 2026Article
- Advances in gene editing tools for four typical Gram-positive bacteria.Frontiers in microbiology · 2026Review
- Multi-targeting zinc finger nuclease vector unsilences paternal UBE3A in a mouse model of Angelman syndrome.Gene therapy · 2026Article
- Dynamic Assemblies in Genome Maintenance.Advances in experimental medicine and biology · 2026Review
- Time-Resolved Fluorescence Detection of Nicked DNA via Site-Specific Stacking of Sulfo-Cy3: The Role of Charge, Polarity, Linker, and Sequence Context.The journal of physical chemistry. B · 2025Article
- The editable landscape of the yeast genome reveals hotspots of structural variant formation.Science advances · 2025Article
- Autophagy induction enhances homologous recombination-associated CRISPR-Cas9 gene editing.Nucleic acids research · 2025Article
- Targeting BRCA1-deficient PARP inhibitor-resistant cells with nickases reveals nick resection as a cancer vulnerability.Nature cancer · 2025Article
- Two-ended recombination at a Flp-nickase-broken replication fork.Molecular cell · 2025Article
- Mechanisms of tandem duplication in the cancer genome.DNA repair · 2025Review
- Recurrent DNA nicks drive massive expansions of (GAA)Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- One-ended and two-ended breaks at nickase-broken replication forks.DNA repair · 2024Review
- Integration of CRISPR/Cas9 with multi-omics technologies to engineer secondary metabolite productions in medicinal plant: Challenges and Prospects.Functional & integrative genomics · 2024Review
- Review
- Enhancing homology-directed repair efficiency with HDR-boosting modular ssDNA donor.Nature communications · 2024Article
- Outlook on genome editing application to cattle.Journal of veterinary science · 2024Review
68 more citing papers are in PubMed but not listed here.
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 1 institution in 1 country.
Funding
Abstract
DNA nicks are the most common form of DNA damage, and if unrepaired can give rise to genomic instability. In human cells, nicks are efficiently repaired via the single-strand break repair pathway, but relatively little is known about the fate of nicks not processed by that pathway. Here we show that homology-directed repair (HDR) at nicks occurs via a mechanism distinct from HDR at double-strand breaks (DSBs). HDR at nicks, but not DSBs, is associated with transcription and is eightfold more efficient at a nick on the transcribed strand than at a nick on the nontranscribed strand. HDR at nicks can proceed by a pathway dependent upon canonical HDR factors RAD51 and BRCA2; or by an efficient alternative pathway that uses either ssDNA or nicked dsDNA donors and that is strongly inhibited by RAD51 and BRCA2. Nicks generated by either I-AniI or the CRISPR/Cas9(D10A) nickase are repaired by the alternative HDR pathway with little accompanying mutagenic end-joining, so this pathway may be usefully applied to genome engineering. These results suggest that alternative HDR at nicks may be stimulated in physiological contexts in which canonical RAD51/BRCA2-dependent HDR is compromised or down-regulated, which occurs frequently in tumors.
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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.