Evidence map›Paper›PMID 28981887›Full record

ArticleNucleic acids research2017

Molecular mechanisms by which oxidative DNA damage promotes telomerase activity.

Hui-Ting Lee, Arindam Bose, Chun-Ying Lee, Patricia L Opresko, Sua Myong

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

51 citing papers in PubMed, 74 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Oxidative Stress and DNA Damage at Telomeres.Cold Spring Harbor perspectives in biology · 2025
    Review
  7. Electroanalytical Quantification of DNA Chirality.Langmuir : the ACS journal of surfaces and colloids · 2024
    Article
  8. Review
  9. Dynamic Structures and Fast Transition Kinetics of Oxidized G-Quadruplexes.Small (Weinheim an der Bergstrasse, Germany) · 2024
    Article
  10. Article
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Review
  17. Review
  18. Crosstalk between G-quadruplex and ROS.Cell death & disease · 2023
    Review
  19. Article
  20. Article
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.

Hui-Ting LeeThomas C. Jenkins Department of Biophysics, Johns Hopkins University, Baltimore, MD, 21218, USA.
Arindam BoseDepartment of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health and UPMC Hillman Cancer Center, Pittsburgh, PA 15261, USA.
Chun-Ying LeeThomas C. Jenkins Department of Biophysics, Johns Hopkins University, Baltimore, MD, 21218, USA.
Patricia L OpreskoDepartment of Environmental and Occupational Health, University of Pittsburgh Graduate School of Public Health and UPMC Hillman Cancer Center, Pittsburgh, PA 15261, USA.
Sua MyongThomas C. Jenkins Department of Biophysics, Johns Hopkins University, Baltimore, MD, 21218, USA.
Johns Hopkins University · USUPMC Hillman Cancer Center · USUrbana University · US

Funding

Roles of Telomeric Oxidative DNA Lesions in Telomere Length RegulationR01CA207342 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Sua Myong, Patricia L Opresko · 2017 to 2026
$3.7M
Mechanisms of Telomere Resistance to DNA Lesion RemovalR01ES022944 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L · 2013 to 2017
$1.6M
NCI NIH HHS R01 CA207342NIEHS NIH HHS R01 ES022944
6 · The paper itself

Abstract

Telomeres are highly susceptible to oxidative DNA damage, which if left unrepaired can lead to dysregulation of telomere length homeostasis. Here we employed single molecule FRET, single molecule pull-down and biochemical analysis to investigate how the most common oxidative DNA lesions, 8-oxoguanine (8oxoG) and thymine glycol (Tg), regulate the structural properties of telomeric DNA and telomerase extension activity. In contrast to 8oxoG which disrupts the telomeric DNA structure, Tg exhibits substantially reduced perturbation of G-quadruplex folding. As a result, 8oxoG induces high accessibility, whereas Tg retains limited accessibility, of telomeric G-quadruplex DNA to complementary single stranded DNA and to telomere binding protein POT1. Surprisingly, the Tg lesion stimulates telomerase loading and activity to a similar degree as an 8oxoG lesion. We demonstrate that this unexpected stimulation arises from Tg-induced conformational alterations and dynamics in telomeric DNA. Despite impacting structure by different mechanisms, both 8oxoG and Tg enhance telomerase binding and extension activity to the same degree, potentially contributing to oncogenesis.

Indexed as

DNA DamageOxidative StressBase SequenceDNADNA, Single-StrandedG-QuadruplexesGuanineHEK293 CellsHumansProtein BindingShelterin ComplexTelomeraseTelomereTelomere-Binding ProteinsTelomere HomeostasisThymine8-hydroxyguanineDNADNA, Single-StrandedGuaninePOT1 protein, humanShelterin ComplexTelomeraseTelomere-Binding ProteinsThyminethymine glycol

Identifiers

PMID28981887
PMCPMC5714237
OpenAlexW2755501245

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.