Evidence map›Paper›PMID 17015833›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2006

A role for WRN in telomere-based DNA damage responses.

Mark S Eller, Xiaodong Liao, SuiYang Liu, Kendra Hanna, Helena Bäckvall, Patricia L Opresko, Vilhelm A Bohr, Barbara A Gilchrest

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
5.5field-weighted citation impact, top 4% 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

28 citing papers in PubMed, 65 citations in OpenAlex.

  1. Synergistic Effects of Solar Exposure and Skin Sensitivity on Skin Aging: A Clinical Study Using Multimodal Noninvasive Measurements.Skin research and technology : official journal of International Society for Bioengineering and the Skin (ISBS) [and] International Society for Digital Imaging of Skin (ISDIS) [and] International Society for Skin Imaging (ISSI) · 2026
    Observational
  2. Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Treating Cancer by Targeting Telomeres and Telomerase.Antioxidants (Basel, Switzerland) · 2017
    Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. DNA damage to a single chromosome end delays anaphase onset.The Journal of biological chemistry · 2014
    Article
  13. Beyond Telomerase: Telomere Instability as a Novel Target for Cancer Therapy.Journal of molecular and genetic medicine : an international journal of biomedical research · 2013
    Article
  14. Article
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  18. Article
  19. Review
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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

8 authors at 3 institutions in 1 country.

Mark S EllerDepartment of Dermatology, Boston University School of Medicine, 609 Albany Street, Boston, MA 02118, USA.
Xiaodong Liao
SuiYang Liu
Kendra Hanna
Helena Bäckvall
Patricia L Opresko
Vilhelm A Bohr
Barbara A Gilchrest
Boston University · USNational Institute on Aging · USUniversity of Pittsburgh · US

Funding

Function of RecQ helicases in genome stabilityZIAAG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$13.1M
Function of RecQ helicases in genome stabilityZ01AG000726 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1993 to 2008
$2.9M
6 · The paper itself

Abstract

Telomeres cap the ends of eukaryotic chromosomes and prevent them from being recognized as DNA breaks. We have shown that certain DNA damage responses induced during senescence and, at times of telomere uncapping, also can be induced by treatment of cells with small DNA oligonucleotides homologous to the telomere 3' single-strand overhang (T-oligos), implicating this overhang in generation of these telomere-based damage responses. Here, we show that T-oligo-treated fibroblasts contain gammaH2AX foci and that these foci colocalize with telomeres. T-oligos with nuclease-resistant 3' ends are inactive, suggesting that a nuclease initiates T-oligo responses. We therefore examined WRN, a 3'-->5' exonuclease and helicase mutated in Werner syndrome, a disorder characterized by aberrant telomere maintenance, premature aging, chromosomal rearrangements, and predisposition to malignancy. Normal fibroblasts and U20S osteosarcoma cells rendered deficient in WRN showed reduced phosphorylation of p53 and histone H2AX in response to T-oligo treatment. Together, these data demonstrate a role for WRN in processing of telomeric DNA and subsequent activation of DNA damage responses. The T-oligo model helps define the role of WRN in telomere maintenance and initiation of DNA damage responses after telomere disruption.

Indexed as

DNA DamageDNA RepairCells, CulturedCellular SenescenceExodeoxyribonucleasesHumansInfant, NewbornOligodeoxyribonucleotidesRecQ HelicasesTelomereWerner SyndromeWerner Syndrome HelicaseExodeoxyribonucleasesOligodeoxyribonucleotidesoligo (dT)RecQ HelicasesWerner Syndrome HelicaseWRN protein, human

Identifiers

PMID17015833
PMCPMC1586178
OpenAlexW2017933374

What OpenQuestion holds

Textmetadata
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.