ArticleMolecular and cellular biology2004
Telomere shortening exposes functions for the mouse Werner and Bloom syndrome genes.
Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 113 papers, 1 of them a synthesis that pooled it.
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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
113 citing papers in PubMed, 1 synthesis or guideline pooled it, 210 citations in OpenAlex.
- Meta-analyses identify 13 loci associated with age at menopause and highlight DNA repair and immune pathways.Nature genetics · 2012Pooled it
- Somatic mutations and genome mosaicism in aging and disease.Experimental & molecular medicine · 2026Review
- Loss of DHX36/G4R1, a G4 resolvase, drives genome instability and regulates innate immune gene expression in cancer cells.Nucleic acids research · 2025Article
- p21 Regulates Wnt-Notch balance via DREAM/MMB/Rb-E2F1 and maintains intestinal stem cell homeostasis.Cell death discovery · 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
- WRN exonuclease imparts high fidelity on translesion synthesis by Y family DNA polymerases.Genes & development · 2024Article
- Telomeres: Dysfunction, Maintenance, Aging and Cancer.Aging and disease · 2023Review
- Telomere length as a predictive biomarker in osteoporosis (Review).Biomedical reports · 2023Review
- Modified iPOND revealed the role of mutant p53 in promoting helicase function and telomere maintenance.Aging · 2023Article
- Interactions between the DNA Damage Response and the Telomere Complex in Carcinogenesis: A Hypothesis.Current issues in molecular biology · 2023Review
- "Bone-SASP" in Skeletal Aging.Calcified tissue international · 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
- Mammalian Resilience Revealed by a Comparison of Human Diseases and Mouse Models Associated With DNA Helicase Deficiencies.Frontiers in molecular biosciences · 2022Review
- Review
- Synthetic Lethal Interactions of RECQ Helicases.Trends in cancer · 2021Review
- Review
- Molecular Aspects of Senescence and Organismal Ageing-DNA Damage Response, Telomeres, Inflammation and Chromatin.International journal of molecular sciences · 2021Review
- Premature Ovarian Insufficiency: Past, Present, and Future.Frontiers in cell and developmental biology · 2021Review
- Telomere damage induces internal loops that generate telomeric circles.Nature communications · 2020Article
53 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Werner and Bloom syndromes are caused by loss-of-function mutations in WRN and BLM, respectively, which encode the RecQ family DNA helicases WRN and BLM, respectively. Persons with Werner syndrome displays premature aging of the skin, vasculature, reproductive system, and bone, and those with Bloom syndrome display more limited features of aging, including premature menopause; both syndromes involve genome instability and increased cancer. The proteins participate in recombinational repair of stalled replication forks or DNA breaks, but the precise functions of the proteins that prevent rapid aging are unknown. Accumulating evidence points to telomeres as targets of WRN and BLM, but the importance in vivo of the proteins in telomere biology has not been tested. We show that Wrn and Blm mutations each accentuate pathology in later-generation mice lacking the telomerase RNA template Terc, including acceleration of phenotypes characteristic of latest-generation Terc mutants. Furthermore, pathology not observed in Terc mutants but similar to that observed in Werner syndrome and Bloom syndrome, such as bone loss, was observed. The pathology was accompanied by enhanced telomere dysfunction, including end-to-end chromosome fusions and greater loss of telomere repeat DNA compared with Terc mutants. These findings indicate that telomere dysfunction may contribute to the pathogenesis of Werner syndrome and Bloom 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.