ArticleAging2010
Cooperation of DNA-PKcs and WRN helicase in the maintenance of telomeric D-loops.
Article in Aging, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
The trial behind it
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
24 citing papers in PubMed.
- DNA-PK controls Apollo's access to leading-end telomeres.Nucleic acids research · 2024Article
- Telomere maintenance and the DNA damage response: a paradoxical alliance.Frontiers in cell and developmental biology · 2024Article
- RecQ Helicase Somatic Alterations in Cancer.Frontiers in molecular biosciences · 2022Review
- CDK2 phosphorylation of Werner protein (WRN) contributes to WRN's DNA double-strand break repair pathway choice.Aging cell · 2021Article
- Structure of the helicase core of Werner helicase, a key target in microsatellite instability cancers.Life science alliance · 2021Article
- RecQ helicases in DNA repair and cancer targets.Essays in biochemistry · 2020Review
- DNA-dependent protein kinase in telomere maintenance and protection.Cellular & molecular biology letters · 2020Review
- Either Rap1 or Cdc13 can protect telomeric single-stranded 3' overhangs from degradation in vitro.Scientific reports · 2019Article
- Different non-synonymous polymorphisms modulate the interaction of the WRN protein to its protein partners and its enzymatic activities.Oncotarget · 2016Article
- Human RecQ helicases in DNA repair, recombination, and replication.Annual review of biochemistry · 2014Review
- DNA-PKcs inhibition sensitizes cancer cells to carbon-ion irradiation via telomere capping disruption.PloS one · 2013Article
- Chromatin structure in telomere dynamics.Frontiers in oncology · 2013Article
- Potential anti-aging agents suppress the level of constitutive mTOR- and DNA damage- signaling.Aging · 2012Article
- Controversial aspects of oncogene-induced senescence.Cell cycle (Georgetown, Tex.) · 2012Review
- Chromatin remodeling, DNA damage repair and aging.Current genomics · 2012Article
- CDK1 differentially regulates G-overhang generation at leading- and lagging-strand telomeres in telomerase-negative cells in G2 phase.Cell cycle (Georgetown, Tex.) · 2012Article
- Werner syndrome protein suppresses the formation of large deletions during the replication of human telomeric sequences.Cell cycle (Georgetown, Tex.) · 2012Article
- RecQ helicases in DNA double strand break repair and telomere maintenance.Mutation research · 2012Review
- Telomerase-independent paths to immortality in predictable cancer subtypes.Journal of Cancer · 2012Article
- Helicase-inactivating mutations as a basis for dominant negative phenotypes.Cell cycle (Georgetown, Tex.) · 2010Review
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Werner syndrome is an inherited human progeriod syndrome caused by mutations in the gene encoding the Werner Syndrome protein, WRN. It has both 3'-5' DNA helicase and exonuclease activities, and is suggested to have roles in many aspects of DNA metabolism, including DNA repair and telomere maintenance. The DNA-PK complex also functions in both DNA double strand break repair and telomere maintenance. Interaction between WRN and the DNA-PK complex has been reported in DNA double strand break repair, but their possible cooperation at telomeres has not been reported. This study analyzes thein vitro and in vivo interaction at the telomere between WRN and DNA-PKcs, the catalytic subunit of DNA-PK. The results show that DNA-PKcs selectively stimulates WRN helicase but not WRN exonuclease in vitro, affecting that WRN helicase unwinds and promotes the release of the full-length invading strand of a telomere D-loop model substrate. In addition, the length of telomeric G-tails decreases in DNA-PKcs knockdown cells, and this phenotype is reversed by overexpression of WRN helicase. These results suggest that WRN and DNA-PKcs may cooperatively prevent G-tail shortening in vivo.
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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.