Evidence map›Paper›PMID 26420422›Full record

ArticleNature communications2015

The DNA structure and sequence preferences of WRN underlie its function in telomeric recombination events.

Deanna N Edwards, Amrita Machwe, Li Chen, Vilhelm A Bohr, David K Orren

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.4field-weighted citation impact, top 19% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

15 citing papers in PubMed, 21 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Review
  8. Article
  9. Werner Syndrome Protein and DNA Replication.International journal of molecular sciences · 2018
    Review
  10. TheThe Journal of biological chemistry · 2018
    Article
  11. Article
  12. Review
  13. Article
  14. Single-molecule imaging reveals a common mechanism shared by G-quadruplex-resolving helicases.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  15. G-quadruplexes and helicases.Nucleic acids research · 2016
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 1 country.

Deanna N EdwardsDepartment of Toxicology and Cancer Biology, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA.
Amrita MachweDepartment of Toxicology and Cancer Biology, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA.
Li ChenMarkey Cancer Center, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, Maryland 21224, USA.
David K OrrenDepartment of Toxicology and Cancer Biology, University of Kentucky College of Medicine, Lexington, Kentucky 40536, USA.
University of Kentucky · USMarkey Cancer Center · USNational Institutes of Health · US

Funding

University of Kentucky Markey Cancer Center Support Grant ECIA SupplementP30CA177558 · NCI · UNIVERSITY OF KENTUCKY · PI KATHLEEN L. O'CONNOR · 2013 to 2026
$38.3M
Function of RecQ helicases in genome stabilityZIAAG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$13.1M
The Function of Werner Syndrome ProteinZIAAG000721 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$7.7M
TRAINING GRANT IN MOLECULAR MECHANISMS OF TOXICITY.T32ES007266 · NIEHS · UNIVERSITY OF KENTUCKY · PI LIU, XIAOQI, MELLON, ISABEL W · 1990 to 2020
$3.7M
Telomeric dysfunction and the premature aging and cancer-prone disease Werner synR01AG027258 · NIA · UNIVERSITY OF KENTUCKY · PI ORREN, DAVID KEITH · 2008 to 2011
$947k
Intramural NIH HHSNCI NIH HHS P30 CA177558NCI NIH HHS P30CA177558NIA NIH HHS AG027258NIA NIH HHS R01 AG027258NIEHS NIH HHS T32 ES007266NIEHS NIH HHS T32ES007266
6 · The paper itself

Abstract

Telomeric abnormalities caused by loss of function of the RecQ helicase WRN are linked to the multiple premature ageing phenotypes that characterize Werner syndrome. Here we examine WRN's role in telomeric maintenance, by comparing its action on a variety of DNA structures without or with telomeric sequences. Our results show that WRN clearly prefers to act on strand invasion intermediates in a manner that favours strand invasion and exchange. Moreover, WRN unwinding of these recombination structures is further enhanced when the invading strand contains at least three G-rich single-stranded telomeric repeats. These selectivities are most pronounced at NaCl concentrations within the reported intranuclear monovalent cation concentration range, and are partly conferred by WRN's C-terminal region. Importantly, WRN's specificity for the G-rich telomeric sequence within this precise structural context is particularly relevant to telomere metabolism and strongly suggests a physiological role in telomeric recombination processes, including T-loop dynamics.

Indexed as

Recombination, GeneticDNAExodeoxyribonucleasesHumansRecQ HelicasesTelomereWerner SyndromeWerner Syndrome HelicaseDNAExodeoxyribonucleasesRecQ HelicasesWerner Syndrome HelicaseWRN protein, human

Identifiers

PMID26420422
PMCPMC4589872
OpenAlexW2265283765

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.