ArticleCell reports2014
Nonenzymatic role for WRN in preserving nascent DNA strands after replication stress.
Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 73 citations in OpenAlex.
- Homozygosity for the WRN Helicase-Inactivating Variant, R834C, does not confer a Werner syndrome clinical phenotype.Scientific reports · 2017Trial
- Carbon ion irradiation at a clinically used dose rewires super-enhancers to drive necroptosis and systemic immunity.Science advances · 2026Article
- Structural basis of Ku-mediated activation of WRN exonuclease activity.Nature communications · 2026Article
- A mutational scar-based genome-wide map of DNA double-strand break repair.Nature communications · 2026Article
- PLK1 phosphorylates WRN at replication forks.The Journal of pharmacology and experimental therapeutics · 2025Article
- USP50 suppresses alternative RecQ helicase use and deleterious DNA2 activity during replication.Nature communications · 2024Article
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- Replication stress as a driver of cellular senescence and aging.Communications biology · 2024Review
- Single-molecule imaging of genome maintenance proteins encountering specific DNA sequences and structures.DNA repair · 2023Review
- A non-catalytic N-terminus domain of WRN prevents mitotic telomere deprotection.Scientific reports · 2023Article
- Werner syndrome protein works as a dimer for unwinding and replication fork regression.Nucleic acids research · 2023Article
- WRN Is a Promising Synthetic Lethal Target for Cancers with Microsatellite Instability (MSI).Cancer treatment and research · 2023Article
- Review
- 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
- NBS1-CtIP-mediated DNA end resection suppresses cGAS binding to micronuclei.Nucleic acids research · 2022Article
- WRN helicase safeguards deprotected replication forks in BRCA2-mutated cancer cells.Nature communications · 2021Article
- Checkpoint functions of RecQ helicases at perturbed DNA replication fork.Current genetics · 2021Review
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Type I Interferon Induction in Cutaneous DNA Damage Syndromes.Frontiers in immunology · 2021Review
- Replication Fork Reversal and Protection.Frontiers in cell and developmental biology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
WRN, the protein defective in Werner syndrome (WS), is a multifunctional nuclease involved in DNA damage repair, replication, and genome stability maintenance. It was assumed that the nuclease activities of WRN were critical for these functions. Here, we report a nonenzymatic role for WRN in preserving nascent DNA strands following replication stress. We found that lack of WRN led to shortening of nascent DNA strands after replication stress. Furthermore, we discovered that the exonuclease activity of MRE11 was responsible for the shortening of newly replicated DNA in the absence of WRN. Mechanistically, the N-terminal FHA domain of NBS1 recruits WRN to replication-associated DNA double-stranded breaks to stabilize Rad51 and to limit the nuclease activity of its C-terminal binding partner MRE11. Thus, this previously unrecognized nonenzymatic function of WRN in the stabilization of nascent DNA strands sheds light on the molecular reason for the origin of genome instability in WS individuals.
Indexed as
Identifiers
What OpenQuestion holds
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.