ArticleCell cycle (Georgetown, Tex.)2012
Werner syndrome protein suppresses the formation of large deletions during the replication of human telomeric sequences.
Article in Cell cycle (Georgetown, Tex.), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 53 citations in OpenAlex.
- Rare genetic diseases associated with G-quadruplex-induced replication stress.Communications biology · 2026Review
- 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
- Werner helicase interacting protein 1 contributes to G-quadruplex processing in human cells.Scientific reports · 2024Article
- Conservation of the insert-2 motif confers Rev1 from different species with an ability to disrupt G-quadruplexes and stimulate translesion DNA synthesis.RSC chemical biology · 2023Article
- Conserved G-Quadruplex-Forming Sequences in MammalianLife (Basel, Switzerland) · 2023Article
- Non-canonical DNA structures: Diversity and disease association.Frontiers in genetics · 2022Review
- The DHX36-specific-motif (DSM) enhances specificity by accelerating recruitment of DNA G-quadruplex structures.Biological chemistry · 2021Review
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- Human Rev1 relies on insert-2 to promote selective binding and accurate replication of stabilized G-quadruplex motifs.Nucleic acids research · 2021Article
- Roles for the 8-Oxoguanine DNA Repair System in Protecting Telomeres From Oxidative Stress.Frontiers in cell and developmental biology · 2021Review
- Review
- Article
- Replication of G Quadruplex DNA.Genes · 2019Review
- TheThe Journal of biological chemistry · 2018Article
- Yeast Hrq1 shares structural and functional homology with the disease-linked human RecQ4 helicase.Nucleic acids research · 2017Article
- Residues in the RecQ C-terminal Domain of the Human Werner Syndrome Helicase Are Involved in Unwinding G-quadruplex DNA.The Journal of biological chemistry · 2017Article
- Recent Advances in Understanding Werner Syndrome.F1000Research · 2017Review
- Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions.Ageing research reviews · 2017Review
- WRN regulates pathway choice between classical and alternative non-homologous end joining.Nature communications · 2016Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Werner syndrome (WS) is a disorder characterized by features of premature aging and increased cancer that is caused by loss of the RecQ helicase WRN. Telomeres consisting of duplex TTAGGG repeats in humans protect chromosome ends and sustain cellular proliferation. WRN prevents the loss of telomeres replicated from the G-rich strand, which can form secondary G-quadruplex (G4) structures. Here, we dissected WRN roles in the replication of telomeric sequences by examining factors inherent to telomeric repeats, such as G4 DNA, independently from other factors at chromosome ends that can also impede replication. For this we used the supF shuttle vector (SV) mutagenesis assay. We demonstrate that SVs with [TTAGGG]6 sequences are stably replicated in human cells, and that the repeats suppress the frequency of large deletions despite G4 folding potential. WRN depletion increased the supF mutant frequency for both the telomeric and non-telomeric SVs, compared with the control cells, but this increase was much greater (27-fold) for telomeric SVs. The higher SV mutant frequencies in WRN-deficient cells were primarily due to an increase in large sequence deletions and rearrangements. However, WRN depletion caused a more dramatic increase in deletions and rearrangements arising within the telomeric SV (70-fold), compared with non-telomeric SV (8-fold). Our results indicate that WRN prevents large deletions and rearrangements during replication, and that this role is particularly important in templates with telomeric sequence. This provides a possible explanation for increased telomere loss in WS cells.
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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.