Evidence map›Paper›PMID 27233113›Full record

ReviewDNA repair2016

DNA damage processing at telomeres: The ends justify the means.

Elise Fouquerel, Dhvani Parikh, Patricia Opresko

Abstract readReview
In one paragraph

Review in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
–field-weighted citation impact
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

31 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Research progress on the role of the NEIL family in cancer.Frontiers in cell and developmental biology · 2025
    Review
  6. Article
  7. Review
  8. Article
  9. Article
  10. Review
  11. Crosstalk between G-quadruplex and ROS.Cell death & disease · 2023
    Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

3 authors.

Elise FouquerelDepartment of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, University of Pittsburgh Cancer Institute Research Pavilion, 5117 Centre Avenue, University of Pittsburgh, Pittsburgh, PA 15213, United States.
Dhvani ParikhDepartment of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, University of Pittsburgh Cancer Institute Research Pavilion, 5117 Centre Avenue, University of Pittsburgh, Pittsburgh, PA 15213, United States.
Patricia OpreskoDepartment of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health, University of Pittsburgh Cancer Institute Research Pavilion, 5117 Centre Avenue, University of Pittsburgh, Pittsburgh, PA 15213, United States. Electronic address: plo4@pitt.edu.

Funding

Mechanisms of Telomere Resistance to DNA Lesion RemovalR01ES022944 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L · 2013 to 2017
$1.6M
ROS driven mitochondrial-telomere dysfunction during environmental stressR33ES025606 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L, VAN HOUTEN, BENNETT · 2017 to 2019
$1.6M
GammaPNA Miniprobes for Telomere FISHR43GM108187 · NIGMS · PNA INNOVATIONS, INC. · PI ARMITAGE, BRUCE A., OPRESKO, PATRICIA L · 2013 to 2014
$541k
Oxidative DNA base damage and repair at telomeres and the relevance to cell senesR21AG045545 · NIA · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI LAN, LI, OPRESKO, PATRICIA L · 2013 to 2014
$422k
NIA NIH HHS R21 AG045545NIEHS NIH HHS R01 ES022944NIEHS NIH HHS R33 ES025606NIGMS NIH HHS R43 GM108187
6 · The paper itself

Abstract

Telomeres at chromosome ends are nucleoprotein structures consisting of tandem TTAGGG repeats and a complex of proteins termed shelterin. DNA damage and repair at telomeres is uniquely influenced by the ability of telomeric DNA to form alternate structures including loops and G-quadruplexes, coupled with the ability of shelterin proteins to interact with and regulate enzymes in every known DNA repair pathway. The role of shelterin proteins in preventing telomeric ends from being falsely recognized and processed as DNA double strand breaks is well established. Here we focus instead on recent developments in understanding the roles of shelterin proteins and telomeric DNA sequence and structure in processing genuine damage at telomeres induced by endogenous and exogenous DNA damage agents. We will highlight advances in double strand break repair, base excision repair and nucleotide excision repair at telomeres, and will discuss important questions remaining in the field.

Indexed as

DNA RepairDNA ReplicationAnimalsDNADNA Breaks, Double-StrandedDNA GlycosylasesG-QuadruplexesHumansProtein SubunitsShelterin ComplexTelomereTelomere-Binding ProteinsTelomere HomeostasisDNADNA GlycosylasesNEIL1 protein, humanProtein SubunitsShelterin ComplexTelomere-Binding ProteinsBase excision repairDNA damageDNA repairDouble strand break repairG-quadruplexNucleotide excision repairShelterin proteinsTelomeres

Identifiers

PMID27233113
PMCPMC9926531

What OpenQuestion holds

Textmetadata
LicenceTDM
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.