ArticleGenes & development2005
Elevated telomere-telomere recombination in WRN-deficient, telomere dysfunctional cells promotes escape from senescence and engagement of the ALT pathway.
Article in Genes & development, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 99 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.
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Who cites it
99 citing papers in PubMed, 189 citations in OpenAlex.
- Tumorigenic p53N236S balances aging and tumorigenesis via regulating DREAM/MMB and downstream telomere DNA replication pathways.Journal of molecular cell biology · 2026Article
- Alternative Lengthening of Telomeres: The Need forInternational journal of molecular sciences · 2025Article
- Whole Exome Sequencing Identifies a Novel Frameshift Mutation of the WRN Gene in a Werner Syndrome Family and Functional Analysis.Molecular genetics & genomic medicine · 2025Article
- Multiple functions of the ALT favorite helicase, BLM.Cell & bioscience · 2025Review
- Interplay between epigenetics, senescence and cellular redox metabolism in cancer and its therapeutic implications.Redox biology · 2024Review
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- The dual role of the DREAM/G2M pathway in non-tumorigenic immortalization of senescent cells.FEBS open bio · 2024Article
- Modified iPOND revealed the role of mutant p53 in promoting helicase function and telomere maintenance.Aging · 2023Article
- The Molecular Mechanisms and Therapeutic Prospects of Alternative Lengthening of Telomeres (ALT).Cancers · 2023Review
- WRN rescues replication forks compromised by a BRCA2 deficiency: Predictions for how inhibition of a helicase that suppresses premature aging tilts the balance to fork demise and chromosomal instability in cancer.BioEssays : news and reviews in molecular, cellular and developmental biology · 2022Article
- Regulation of telomere homeostasis and genomic stability in cancer byScience advances · 2021Article
- Extrachromosomal circular DNA: a new potential role in cancer progression.Journal of translational medicine · 2021Review
- Human WRN is an intrinsic inhibitor of progerin, abnormal splicing product of lamin A.Scientific reports · 2021Article
- Article
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Crosstalk among DNA Damage, Mitochondrial Dysfunction, Impaired Mitophagy, Stem Cell Attrition, and Senescence in the Accelerated Ageing Disorder Werner Syndrome.Cytogenetic and genome research · 2021Review
- The Distinct Function of p21Frontiers in genetics · 2021Article
- Twenty years of t-loops: A case study for the importance of collaboration in molecular biology.DNA repair · 2020Review
- History of DNA Helicases.Genes · 2020Review
- ATRX affects the repair of telomeric DSBs by promoting cohesion and a DAXX-dependent activity.PLoS biology · 2020Article
39 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
Abstract
Werner Syndrome (WS) is characterized by premature aging, genomic instability, and cancer. The combined impact of WRN helicase deficiency and limiting telomere reserves is central to disease pathogenesis. Here, we report that cells doubly deficient for telomerase and WRN helicase show chromosomal aberrations and elevated recombination rates between telomeres of sister chromatids. Somatic reconstitution of WRN function, but not a WRN helicase-deficient mutant, abolished telomere sister chromatid exchange (T-SCE), indicating that WRN normally represses T-SCEs. Elevated T-SCE was associated with greater immortalization potential and resultant tumors maintained telomeres via the alternative lengthening of telomere (ALT) pathway. We propose that the increased incidence of chromosomal instability and cancer in WS relates in part to aberrant recombinations between sister chromatids at telomeres, which facilitates the activation of ALT and engenders cancer-relevant chromosomal aberrations and tumor formation.
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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.