ArticleNucleic acids research2002
Displacement of DNA-PKcs from DNA ends by the Werner syndrome protein.
Article in Nucleic acids research, 2002. 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
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 64 citations in OpenAlex.
- WRN Is a Promising Synthetic Lethal Target for Cancers with Microsatellite Instability (MSI).Cancer treatment and research · 2023Article
- Latin American Study of Hereditary Breast and Ovarian CancerFrontiers in oncology · 2019Article
- The Werner Syndrome Helicase Coordinates Sequential Strand Displacement and FEN1-Mediated Flap Cleavage during Polymerase δ Elongation.Molecular and cellular biology · 2017Article
- Werner syndrome protein positively regulates XRCC4-like factor transcription.Molecular medicine reports · 2014Article
- Identification and functional characterization of a Ku-binding motif in aprataxin polynucleotide kinase/phosphatase-like factor (APLF).The Journal of biological chemistry · 2013Article
- The role of DNA exonucleases in protecting genome stability and their impact on ageing.Age (Dordrecht, Netherlands) · 2012Review
- RecQ helicases in DNA double strand break repair and telomere maintenance.Mutation research · 2012Review
- RecQ helicases; at the crossroad of genome replication, repair, and recombination.Molecular biology reports · 2012Review
- The HTLV-1 Tax oncoprotein represses Ku80 gene expression.Virology · 2011Article
- Cell cycle-regulated association between the Werner syndrome protein and its molecular partners.Cell cycle (Georgetown, Tex.) · 2011Article
- Depletion of Werner helicase results in mitotic hyperrecombination and pleiotropic homologous and nonhomologous recombination phenotypes.Mechanisms of ageing and development · 2010Article
- Article
- Roles of Werner syndrome protein in protection of genome integrity.DNA repair · 2010Review
- Divergent cellular phenotypes of human and mouse cells lacking the Werner syndrome RecQ helicase.DNA repair · 2010Article
- The mechanism of double-strand DNA break repair by the nonhomologous DNA end-joining pathway.Annual review of biochemistry · 2010Review
- Altered nuclear functions in progeroid syndromes: a paradigm for aging research.TheScientificWorldJournal · 2009Review
- Werner syndrome protein, WRN, protects cells from DNA damage induced by the benzene metabolite hydroquinone.Toxicological sciences : an official journal of the Society of Toxicology · 2009Article
- Article
- Model of human aging: recent findings on Werner's and Hutchinson-Gilford progeria syndromes.Clinical interventions in aging · 2008Review
- Developing master keys to brain pathology, cancer and aging from the structural biology of proteins controlling reactive oxygen species and DNA repair.Neuroscience · 2007Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The DNA-dependent protein kinase (DNA-PK) complex, which is composed of a DNA-dependent kinase subunit (DNA-PKcs) and the Ku70/80 heterodimer, is involved in DNA double-strand break repair by non-homologous end joining (NHEJ). Ku70/80 interacts with the Werner syndrome protein (WRN) and stimulates WRN exonuclease activity. To investigate a possible function of WRN in NHEJ, we have examined the relationship between DNA-PKcs, Ku and WRN. First, we showed that WRN forms a complex with DNA-PKcs and Ku in solution. Next, we determined whether this complex assembles on DNA ends. Interestingly, the addition of WRN to a Ku:DNA-PKcs:DNA complex results in the displacement of DNA-PKcs from the DNA, indicating that the triple complex WRN:Ku:DNA-PKcs cannot form on DNA ends. The displacement of DNA-PKcs from DNA requires the N- and C-terminal regions of WRN, both of which make direct contact with the Ku70/80 heterodimer. Moreover, exonuclease assays indicate that DNA-PKcs does not protect DNA from the nucleolytic action of WRN. These results suggest that WRN may influence the mechanism by which DNA ends are processed.
Indexed as
Identifiers
What OpenQuestion holds
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.