ArticleJournal of cell science2011
WRN helicase regulates the ATR-CHK1-induced S-phase checkpoint pathway in response to topoisomerase-I-DNA covalent complexes.
Article in Journal of cell science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 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
26 citing papers in PubMed, 51 citations in OpenAlex.
- A CHK1-mediated phosphorylation switch suppresses human Topoisomerase 1-associated genomic instability.The EMBO journal · 2026Article
- Coming of age: could obesity-related metabolic complications be treated by targeting senescent cells?Frontiers in cell and developmental biology · 2025Review
- Non-enzymatic function of WRN RECQL helicase regulates removal of topoisomerase-I-DNA covalent complexes and triggers NF-κB signaling in cancer.Aging cell · 2022Article
- A clinically relevant heterozygous ATR mutation sensitizes colorectal cancer cells to replication stress.Scientific reports · 2022Article
- R-Loop-Associated Genomic Instability and Implication of WRN and WRNIP1.International journal of molecular sciences · 2022Review
- CDK2 phosphorylation of Werner protein (WRN) contributes to WRN's DNA double-strand break repair pathway choice.Aging cell · 2021Article
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- RecQ DNA Helicase Rqh1 Promotes Rad3Molecular and cellular biology · 2020Article
- Hepatitis C Virus NS3 Protein Plays a Dual Role in WRN-Mediated Repair of Nonhomologous End Joining.Journal of virology · 2019Article
- ATM pathway activation limits R-loop-associated genomic instability in Werner syndrome cells.Nucleic acids research · 2019Article
- The essential kinase ATR: ensuring faithful duplication of a challenging genome.Nature reviews. Molecular cell biology · 2017Review
- Recombine and Associate to Prevent Genomic Instability and Premature Aging.Molecular syndromology · 2017Article
- CDK1 phosphorylates WRN at collapsed replication forks.Nature communications · 2016Article
- Replication stress: getting back on track.Nature structural & molecular biology · 2016Review
- Mechanisms of Origin, Phenotypic Effects and Diagnostic Implications of Complex Chromosome Rearrangements.Molecular syndromology · 2015Review
- Nonenzymatic role for WRN in preserving nascent DNA strands after replication stress.Cell reports · 2014Article
- Human RecQ helicases in DNA repair, recombination, and replication.Annual review of biochemistry · 2014Review
- Checkpoint regulation of replication forks: global or local?Biochemical Society transactions · 2013Review
- Article
- Distinct functions of human RECQ helicases WRN and BLM in replication fork recovery and progression after hydroxyurea-induced stalling.DNA repair · 2013Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Checkpoints are cellular surveillance and signaling pathways that coordinate the response to DNA damage and replicative stress. Consequently, failure of cellular checkpoints increases susceptibility to DNA damage and can lead to profound genome instability. This study examines the role of a human RECQ helicase, WRN, in checkpoint activation in response to DNA damage. Mutations in WRN lead to genomic instability and the premature aging condition Werner syndrome. Here, the role of WRN in a DNA-damage-induced checkpoint was analyzed in U-2 OS (WRN wild type) and isogenic cells stably expressing WRN-targeted shRNA (WRN knockdown). The results of our studies suggest that WRN has a crucial role in inducing an S-phase checkpoint in cells exposed to the topoisomerase I inhibitor campthothecin (CPT), but not in cells exposed to hydroxyurea. Intriguingly, WRN decreases the rate of replication fork elongation, increases the accumulation of ssDNA and stimulates phosphorylation of CHK1, which releases CHK1 from chromatin in CPT-treated cells. Importantly, knockdown of WRN expression abolished or delayed all these processes in response to CPT. Together, our results strongly suggest an essential regulatory role for WRN in controlling the ATR-CHK1-mediated S-phase checkpoint in CPT-treated cells.
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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.