ArticleThe Journal of cell biology2011
Mus81-mediated DNA cleavage resolves replication forks stalled by topoisomerase I-DNA complexes.
Article in The Journal of cell biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 106 papers.
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
106 citing papers in PubMed, 165 citations in OpenAlex.
- ERCC6 at the Transcription-Replication Interface: Integration of Transcription-Coupled Repair with Replication Stress Responses.International journal of molecular sciences · 2026Review
- R-loop disruption triggers irreversible topoisomerase 1-DNA cleavage complex formation during AID-dependent IgH gene diversification.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Epitranscriptomic RNA editing resolves Mus81 DNA repair tradeoffs in heat tolerance and meiosis.Nature communications · 2026Article
- Discovery of Two Structurally Distinct Classes of Inhibitors Targeting the Nuclease MUS81 and Enhancing Efficacy of Chemotherapy in Cancer Cells.Journal of medicinal chemistry · 2026Article
- How DNA secondary structures drive replication fork instability.DNA repair · 2025Review
- Pathogenic variants in MAEA disrupt DNA replication fork stability and are associated with developmental abnormalities in humans.Science advances · 2025Article
- The polymeric fluoropyrimidine CF10 overcomes limitations of 5-FU in pancreatic ductal adenocarcinoma cells through increased replication stress.Cancer biology & therapy · 2024Article
- Article
- The Fanconi anemia pathway induces chromothripsis and ecDNA-driven cancer drug resistance.Cell · 2024Article
- TDP1 phosphorylation by CDK1 in mitosis promotes MUS81-dependent repair of trapped Top1-DNA covalent complexes.The EMBO journal · 2024Article
- Unprocessed genomic uracil as a source of DNA replication stress in cancer cells.Molecular cell · 2024Article
- Human DNA topoisomerase I poisoning causes R loop-mediated genome instability attenuated by transcription factor IIS.Science advances · 2024Article
- Article
- Chromodomain mutation in S. pombe Kat5/Mst1 affects centromere dynamics and DNA repair.PloS one · 2024Article
- Induction of the alternative lengthening of telomeres pathway by trapping of proteins on DNA.Nucleic acids research · 2023Article
- MUS81 cleaves TOP1-derived lesions and other DNA-protein cross-links.BMC biology · 2023Article
- SMC5/6 complex-mediated SUMOylation stimulates DNA-protein cross-link repair in Arabidopsis.The Plant cell · 2023Article
- FANCD2 promotes mitotic rescue from transcription-mediated replication stress in SETX-deficient cancer cells.Communications biology · 2022Article
- Mechanism of action of non-camptothecin inhibitor Genz-644282 in topoisomerase I inhibition.Communications biology · 2022Article
- TDP1-independent pathways in the process and repair of TOP1-induced DNA damage.Nature communications · 2022Article
46 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
Deoxyribonucleic acid (DNA) topoisomerases are essential for removing the supercoiling that normally builds up ahead of replication forks. The camptothecin (CPT) Top1 (topoisomerase I) inhibitors exert their anticancer activity by reversibly trapping Top1-DNA cleavage complexes (Top1cc's) and inducing replication-associated DNA double-strand breaks (DSBs). In this paper, we propose a new mechanism by which cells avoid Top1-induced replication-dependent DNA damage. We show that the structure-specific endonuclease Mus81-Eme1 is responsible for generating DSBs in response to Top1 inhibition and for allowing cell survival. We provide evidence that Mus81 cleaves replication forks rather than excises Top1cc's. DNA combing demonstrated that Mus81 also allows efficient replication fork progression after CPT treatment. We propose that Mus81 cleaves stalled replication forks, which allows dissipation of the excessive supercoiling resulting from Top1 inhibition, spontaneous reversal of Top1cc, and replication fork progression.
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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.