Evidence map›Paper›PMID 27220469›Full record

ArticleNucleic acids research2016

Widespread transcriptional gene inactivation initiated by a repair intermediate of 8-oxoguanine.

Julia Allgayer, Nataliya Kitsera, Solveig Bartelt, Bernd Epe, Andriy Khobta

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
5.7field-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

52 citing papers in PubMed, 76 citations in OpenAlex.

  1. Structural basis of transcription-coupled RNA damage by incorporation of oxidized ribonucleotides.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  2. Article
  3. 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025
    Review
  4. Review
  5. Review
  6. Article
  7. Review
  8. Review
  9. Review
  10. Article
  11. Article
  12. 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024
    Review
  13. FOXO transcription factors as mediators of stress adaptation.Nature reviews. Molecular cell biology · 2024
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. OGG1 in the Kidney: Beyond Base Excision Repair.Oxidative medicine and cellular longevity · 2022
    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 2 institutions in 1 country.

Julia AllgayerInstitute of Pharmacy and Biochemistry, Johannes Gutenberg University of Mainz, Mainz 55128, Germany.
Nataliya KitseraInstitute of Pharmacy and Biochemistry, Johannes Gutenberg University of Mainz, Mainz 55128, Germany Institute of Toxicology, University Medical Center Mainz, Mainz 55131, Germany.
Solveig BarteltInstitute of Pharmacy and Biochemistry, Johannes Gutenberg University of Mainz, Mainz 55128, Germany.
Bernd EpeInstitute of Pharmacy and Biochemistry, Johannes Gutenberg University of Mainz, Mainz 55128, Germany.
Andriy KhobtaInstitute of Pharmacy and Biochemistry, Johannes Gutenberg University of Mainz, Mainz 55128, Germany Institute of Toxicology, University Medical Center Mainz, Mainz 55131, Germany khobta@uni-mainz.de.
Johannes Gutenberg University Mainz · DEUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

DNA damage can significantly modulate expression of the affected genes either by direct structural interference with transcription components or as a collateral outcome of cellular repair attempts. Thus, DNA glycosylases of the base excision repair (BER) pathway have been implicated in negative transcriptional response to several spontaneously generated DNA base modifications, including a common oxidative DNA base modification 8-oxoguanine (8-oxoG). Here, we report that single 8-oxoG situated in the non-transcribed DNA strand of a reporter gene has a pronounced negative effect on transcription, driven by promoters of various strength and with different structural properties, including viral, human, and artificial promoters. We further show that the magnitude of the negative effect on the gene expression correlates with excision of the modified base by OGG1 in all promoter constructs tested. Moreover, by using expression vectors with nuclease resistant backbone modifications, we demonstrate that OGG1 does not catalyse DNA strand cleavage in vivo. Rather, cleavage of the phosphate bond 5' to 8-oxodG (catalysed by APE1) is essential and universally required for the onset of transcriptional silencing, regardless of the promoter structure. Hence, induction of transcriptional silencing emerges as a ubiquitous mode of biological response to 8-oxoG in DNA.

Indexed as

DNA RepairGene SilencingTranscription, GeneticDNADNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesGuanineHeLa CellsHumansHydroxamic AcidsPlasmidsPromoter Regions, GeneticResponse ElementsSequence Deletion8-hydroxyguanineAPEX1 protein, humanDNADNA-(Apurinic or Apyrimidinic Site) LyaseDNA GlycosylasesGuanineHydroxamic Acidsoxoguanine glycosylase 1, humantrichostatin A

Identifiers

PMID27220469
PMCPMC5009734
OpenAlexW2407364978

What OpenQuestion holds

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LicenceCC BY-NC
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Registered trials

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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.