ArticleProceedings of the National Academy of Sciences of the United States of America2010
Hyper telomere recombination accelerates replicative senescence and may promote premature aging.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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
31 citing papers in PubMed, 53 citations in OpenAlex.
- The crosstalk between telomeres and DNA repair mechanisms: an overview to mammalian somatic cells, germ cells, and preimplantation embryos.Journal of assisted reproduction and genetics · 2024Review
- Exploring the Relationship between Spontaneous Sister Chromatid Exchange and Genome Instability in Two Cryptic Species of Non-Human Primates.Animals : an open access journal from MDPI · 2023Article
- 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
- Roles for Non-coding RNAs in Spatial Genome Organization.Frontiers in cell and developmental biology · 2019Review
- Differential requirements for DNA repair proteins in immortalized cell lines using alternative lengthening of telomere mechanisms.Genes, chromosomes & cancer · 2017Article
- Bloom's syndrome: Why not premature aging?: A comparison of the BLM and WRN helicases.Ageing research reviews · 2017Review
- Convergence of The Nobel Fields of Telomere Biology and DNA Repair.Photochemistry and photobiology · 2017Review
- Werner syndrome: Clinical features, pathogenesis and potential therapeutic interventions.Ageing research reviews · 2017Review
- Nijmegen breakage syndrome fibroblasts expressing the C-terminal truncated NBN(p70) protein undergo p38/MK2-dependent premature senescence.Biogerontology · 2015Article
- Telomeres and Telomerase in the Radiation Response: Implications for Instability, Reprograming, and Carcinogenesis.Frontiers in oncology · 2015Article
- Strand exchange of telomeric DNA catalyzed by the Werner syndrome protein (WRN) is specifically stimulated by TRF2.Nucleic acids research · 2014Article
- Senescence induced by RECQL4 dysfunction contributes to Rothmund-Thomson syndrome features in mice.Cell death & disease · 2014Article
- Rif1 maintains telomere length homeostasis of ESCs by mediating heterochromatin silencing.Developmental cell · 2014Article
- WRN loss induces switching of telomerase-independent mechanisms of telomere elongation.PloS one · 2014Article
- Human RecQ helicases in DNA repair, recombination, and replication.Annual review of biochemistry · 2014Review
- ShaPINg Cell Fate Upon DNA Damage: Role of Pin1 Isomerase in DNA Damage-Induced Cell Death and Repair.Frontiers in oncology · 2014Review
- Article
- The shelterin protein POT-1 anchors Caenorhabditis elegans telomeres through SUN-1 at the nuclear periphery.The Journal of cell biology · 2013Article
- Saccharomyces cerevisiae as a Model to Study Replicative Senescence Triggered by Telomere Shortening.Frontiers in oncology · 2013Article
- Defective repair of oxidative base lesions by the DNA glycosylase Nth1 associates with multiple telomere defects.PLoS genetics · 2013Article
Corrections and comments
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Authors and funding
5 authors at 5 institutions in 2 countries.
Funding
Abstract
Werner syndrome and Bloom syndrome result from defects in the RecQ helicases Werner (WRN) and Bloom (BLM), respectively, and display premature aging phenotypes. Similarly, XFE progeroid syndrome results from defects in the ERCC1-XPF DNA repair endonuclease. To gain insight into the origin of cellular senescence and human aging, we analyzed the dependence of sister chromatid exchange (SCE) frequencies on location [i.e., genomic (G-SCE) vs. telomeric (T-SCE) DNA] in primary human fibroblasts deficient in WRN, BLM, or ERCC1-XPF. Consistent with our other studies, we found evidence of elevated T-SCE in telomerase-negative but not telomerase-positive backgrounds. In telomerase-negative WRN-deficient cells, T-SCE-but not G-SCE-frequencies were significantly increased compared with controls. In contrast, SCE frequencies were significantly elevated in BLM-deficient cells irrespective of genome location. In ERCC1-XPF-deficient cells, neither T- nor G-SCE frequencies differed from controls. A theoretical model was developed that allowed an in silico investigation into the cellular consequences of increased T-SCE frequency. The model predicts that in cells with increased T-SCE, the onset of replicative senescence is dramatically accelerated even though the average rate of telomere loss has not changed. Premature cellular senescence may act as a powerful tumor-suppressor mechanism in telomerase-deficient cells with mutations that cause T-SCE levels to rise. Furthermore, T-SCE-driven premature cellular senescence may be a factor contributing to accelerated aging in Werner and Bloom syndromes, but not XFE progeroid syndrome.
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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.