ArticleNucleic acids research2018
A limited number of double-strand DNA breaks is sufficient to delay cell cycle progression.
Article in Nucleic acids research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 60 papers.
What it found
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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
60 citing papers in PubMed.
- Asymmetric attrition and secondary chromosome destabilization after double-strand breaks in human embryonic development.Nature communications · 2026Article
- Improved in vivo gene knockout with high specificity using multiplexed Cas12a sgRNAs.Nature communications · 2026Article
- Chemically-inducible CRISPR/Cas9 circuits for ultra-high dynamic range gene perturbation.Nature communications · 2025Article
- Engineered chromatin readers track damaged chromatin dynamics in live cells and animals.Nature communications · 2025Article
- ATR promotes genome instability via CENP-A eviction from centromeres under replication stress.bioRxiv : the preprint server for biology · 2025Article
- Coordinated control of genome-nuclear lamina interactions by topoisomerase 2B and lamin B receptor.Nucleic acids research · 2025Article
- Combining Multiplexed CRISPR/Cas9-Nickase and PARP Inhibitors Efficiently and Precisely Targets Cancer Cells.Cancer research · 2025Article
- CRISPR GENome and epigenome engineering improves loss-of-function genetic-screening approaches.Cell reports methods · 2025Article
- Article
- DNA Damage and Replication Stress Checkpoints.Annual review of biochemistry · 2025Review
- Cell-cycle dependent DNA repair and replication unifies patterns of chromosome instability.Nature communications · 2025Article
- Functional genetics reveals modulators of antimicrotubule drug sensitivity.The Journal of cell biology · 2025Article
- Targeting BRCA1-deficient PARP inhibitor-resistant cells with nickases reveals nick resection as a cancer vulnerability.Nature cancer · 2025Article
- CDK12 controls transcription at damaged genes and prevents MYC-induced transcription-replication conflicts.Nature communications · 2024Article
- An aptamer-mediated base editing platform for simultaneous knockin and multiple gene knockout for allogeneic CAR-T cells generation.Molecular therapy : the journal of the American Society of Gene Therapy · 2024Article
- Quantifying DNA replication speeds in single cells by scEdU-seq.Nature methods · 2024Article
- Widespread chromatin context-dependencies of DNA double-strand break repair proteins.Nature communications · 2024Article
- Efficient gene knockout and genetic interaction screening using the in4mer CRISPR/Cas12a multiplex knockout platform.Nature communications · 2024Article
- Duocarmycin SA Reduces Proliferation and Increases Apoptosis in Acute Myeloid Leukemia Cells In Vitro.International journal of molecular sciences · 2024Article
- Functional genetics reveals modulators of anti-microtubule drug sensitivity.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
DNA damaging agents cause a variety of lesions, of which DNA double-strand breaks (DSBs) are the most genotoxic. Unbiased approaches aimed at investigating the relationship between the number of DSBs and outcome of the DNA damage response have been challenging due to the random nature in which damage is induced by classical DNA damaging agents. Here, we describe a CRISPR/Cas9-based system that permits us to efficiently introduce DSBs at defined sites in the genome. Using this system, we show that a guide RNA targeting only a single site in the human genome can trigger a checkpoint response that is potent enough to delay cell cycle progression. Abrogation of this checkpoint leads to DNA breaks in mitosis which gives rise to aneuploid progeny.
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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 Socratic graph.