ArticleHuman genetics2003
Telomere instability in a human tumor cell line expressing a dominant-negative WRN protein.
Article in Human genetics, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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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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.
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Who cites it
27 citing papers in PubMed, 67 citations in OpenAlex.
- Response to Replication Stress and Maintenance of Genome Stability by WRN, the Werner Syndrome Protein.International journal of molecular sciences · 2024Review
- Nijmegen breakage syndrome: 25-year experience of diagnosis and treatment in Ukraine.Frontiers in immunology · 2024Article
- The Werner Syndrome Helicase Coordinates Sequential Strand Displacement and FEN1-Mediated Flap Cleavage during Polymerase δ Elongation.Molecular and cellular biology · 2017Article
- WRN regulates pathway choice between classical and alternative non-homologous end joining.Nature communications · 2016Article
- The DNA structure and sequence preferences of WRN underlie its function in telomeric recombination events.Nature communications · 2015Article
- G4-associated human diseases.EMBO reports · 2015Review
- Strand exchange of telomeric DNA catalyzed by the Werner syndrome protein (WRN) is specifically stimulated by TRF2.Nucleic acids research · 2014Article
- Human RECQL1 participates in telomere maintenance.Nucleic acids research · 2014Article
- The pur protein family: genetic and structural features in development and disease.Journal of cellular physiology · 2013Review
- The roles of WRN and BLM RecQ helicases in the Alternative Lengthening of Telomeres.Nucleic acids research · 2012Article
- QTL Mapping and Candidate Gene Analysis of Telomere Length Control Factors in Maize (Zea mays L.).G3 (Bethesda, Md.) · 2011Article
- Telomere replication: poised but puzzling.Journal of cellular and molecular medicine · 2011Review
- Telomeric repeat mutagenicity in human somatic cells is modulated by repeat orientation and G-quadruplex stability.DNA repair · 2010Article
- Replication protein A stimulates the Werner syndrome protein branch migration activity.The Journal of biological chemistry · 2009Article
- Sequence-specific processing of telomeric 3' overhangs by the Werner syndrome protein exonuclease activity.Aging · 2009Article
- The Werner syndrome helicase/exonuclease processes mobile D-loops through branch migration and degradation.PloS one · 2009Article
- Werner syndrome helicase activity is essential in maintaining fragile site stability.The Journal of cell biology · 2008Article
- Evidence that a RecQ helicase slows senescence by resolving recombining telomeres.PLoS biology · 2007Article
- Telomere dysfunction as a cause of genomic instability in Werner syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Human premature aging, DNA repair and RecQ helicases.Nucleic acids research · 2007Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Werner Syndrome (WS) is an autosomal recessive disease characterized by premature aging and chromosome instability. The protein involved in WS, WRN, is a RecQ-type helicase that also has exonuclease activity. WRN has been demonstrated to bind to a variety of other proteins, including RPA, DNA-PKcs, and TRF2, suggesting that WRN is involved in DNA replication, repair, recombination, and telomere maintenance. In culture, WS cells show premature senescence, which can be overcome by transfection with an expression vector containing the gene for the catalytic subunit of telomerase. However, telomerase expression does not eliminate chromosome instability in WS cells, which led to the proposal that telomere loss is not the cause of the high rate of chromosome rearrangements in WS cells. In the present study, we have investigated how a WRN protein containing a dominant-negative mutation (K577M-WRN) influences the stability of telomeres in a human tumor cell line expressing telomerase. The results demonstrate an increased rate of telomere loss and chromosome fusion in cells expressing K577M-WRN. Expression of K577M-WRN results in reduced levels of telomerase activity, however, the absence of detectable changes in average telomere length demonstrates that WRN-associated telomere loss results from stochastic events involving complete telomere loss or loss of telomere capping function. Thus, telomere loss can contribute to chromosome instability in cells deficient in WRN regardless of the expression of telomerase activity.
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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.