ArticleJournal of molecular biology2008
Bloom's syndrome helicase and Mus81 are required to induce transient double-strand DNA breaks in response to DNA replication stress.
Article in Journal of molecular biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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
53 citing papers in PubMed, 66 citations in OpenAlex.
- 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
- Insights into common fragile site instability: DNA replication challenges at DNA repeat sequences.Emerging topics in life sciences · 2023Article
- Cellular Responses to Widespread DNA Replication Stress.International journal of molecular sciences · 2023Review
- Review
- Nuclear Deformation Causes DNA Damage by Increasing Replication Stress.Current biology : CB · 2021Article
- Article
- Review
- Review
- Article
- Role of PCNA and RFC in promoting Mus81-complex activity.BMC biology · 2017Article
- Replication stalling and DNA microsatellite instability.Biophysical chemistry · 2017Review
- Control of structure-specific endonucleases to maintain genome stability.Nature reviews. Molecular cell biology · 2017Review
- The Intra-S Checkpoint Responses to DNA Damage.Genes · 2017Review
- A replicator-specific binding protein essential for site-specific initiation of DNA replication in mammalian cells.Nature communications · 2016Article
- Evaluating the Role of p38 MAPK in the Accelerated Cell Senescence of Werner Syndrome Fibroblasts.Pharmaceuticals (Basel, Switzerland) · 2016Article
- Article
- Inhibiting WEE1 Selectively Kills Histone H3K36me3-Deficient Cancers by dNTP Starvation.Cancer cell · 2015Article
- The DNA repair endonuclease Mus81 facilitates fast DNA replication in the absence of exogenous damage.Nature communications · 2015Article
- Cooperation of Blm and Mus81 in development, fertility, genomic integrity and cancer suppression.Oncogene · 2015Article
- Fanconi anemia signaling and Mus81 cooperate to safeguard development and crosslink repair.Nucleic acids research · 2014Article
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 2 institutions in 2 countries.
Funding
Abstract
Perturbed DNA replication either activates a cell cycle checkpoint, which halts DNA replication, or decreases the rate of DNA synthesis without activating a checkpoint. Here we report that at low doses, replication inhibitors did not activate a cell cycle checkpoint, but they did activate a process that required functional Bloom's syndrome-associated (BLM) helicase, Mus81 nuclease and ataxia telangiectasia mutated and Rad3-related (ATR) kinase to induce transient double-stranded DNA breaks. The induction of transient DNA breaks was accompanied by dissociation of proliferating cell nuclear antigen (PCNA) and DNA polymerase alpha from replication forks. In cells with functional BLM, Mus81 and ATR, the transient breaks were promptly repaired and DNA continued to replicate at a slow pace in the presence of replication inhibitors. In cells that lacked BLM, Mus81, or ATR, transient breaks did not form, DNA replication did not resume, and exposure to low doses of replication inhibitors was toxic. These observations suggest that BLM helicase, ATR kinase, and Mus81 nuclease are required to convert perturbed replication forks to DNA breaks when cells encounter conditions that decelerate DNA replication, thereby leading to the rapid repair of those breaks and resumption of DNA replication without incurring DNA damage and without activating a cell cycle checkpoint.
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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.