Evidence map›Paper›PMID 25355508›Full record

ArticleNucleic acids research2014

Polymerase η suppresses telomere defects induced by DNA damaging agents.

Hannah Pope-Varsalona, Fu-Jun Liu, Lynda Guzik, Patricia L Opresko

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2014. 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
1.6field-weighted citation impact, top 17% 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, 19 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. G-quadruplex DNA: a novel target for drug design.Cellular and molecular life sciences : CMLS · 2021
    Review
  5. Review
  6. Article
  7. Article
  8. Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017
    Review
  9. Article
  10. Review
  11. Article
  12. Review
  13. Review
  14. Article
  15. 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

4 authors at 1 institution in 1 country.

Hannah Pope-VarsalonaDepartment of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15219, USA.
Fu-Jun LiuDepartment of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15219, USA.
Lynda GuzikMcGowan Institute for Regenerative Medicine, University of Pittsburgh, Pittsburgh, PA 15260, USA.
Patricia L OpreskoDepartment of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, PA 15219, USA Center for Nucleic Acids Science and Technology, Carnegie Mellon University, Pittsburgh, PA 15213, USA plo4@pitt.edu.
University of Pittsburgh · US

Funding

Therapuetic Immune Targeting of EphA2 Expressed by Melanoma & Its Tumor-AssociateP50CA121973 · NCI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KIRKWOOD, JOHN MUNN · 2008 to 2018
$22.9M
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 5P50CA121973NIEHS NIH HHS R01 ES022944NIEHS NIH HHS R01ES022944
6 · The paper itself

Abstract

Telomeres at chromosome ends are normally masked from proteins that signal and repair DNA double strand breaks (DSBs). Bulky DNA lesions can cause DSBs if they block DNA replication, unless they are bypassed by translesion (TLS) DNA polymerases. Here, we investigated roles for TLS polymerase η, (polη) in preserving telomeres following acute physical UVC exposure and chronic chemical Cr(VI) exposure, which both induce blocking lesions. We report that polη protects against cytotoxicity and replication stress caused by Cr(VI), similar to results with ultraviolet C light (UVC). Both exposures induce ataxia telangiectasia and Rad3-related (ATR) kinase and polη accumulation into nuclear foci and localization to individual telomeres, consistent with replication fork stalling at DNA lesions. Polη-deficient cells exhibited greater numbers of telomeres that co-localized with DSB response proteins after exposures. Furthermore, the genotoxic exposures induced telomere aberrations associated with failures in telomere replication that were suppressed by polη. We propose that polη's ability to bypass bulky DNA lesions at telomeres is critical for proper telomere replication following genotoxic exposures.

Indexed as

DNA DamageDNA RepairAtaxia Telangiectasia Mutated ProteinsCell LineCell Line, TransformedCells, CulturedChromiumChromosome AberrationsDNA-Directed DNA PolymeraseDNA ReplicationHumansMutagensSignal TransductionTelomereUltraviolet RaysY-Family DNA PolymerasesAtaxia Telangiectasia Mutated ProteinsATR protein, humanChromiumchromium hexavalent ionDNA-Directed DNA PolymeraseMutagensRad30 proteinY-Family DNA Polymerases

Identifiers

PMID25355508
PMCPMC4245935
OpenAlexW2169703790

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.