Evidence map›Paper›PMID 18359049›Full record

ArticleMutation research2008

Translesion synthesis of 7,8-dihydro-8-oxo-2'-deoxyguanosine by DNA polymerase eta in vivo.

Dong-Hyun Lee, Gerd P Pfeifer

Open access · greenAbstract read
In one paragraph

Article in Mutation research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

34 citing papers in PubMed, 52 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Change over time of the mutagenicity in the lungs ofGenes and environment : the official journal of the Japanese Environmental Mutagen Society · 2018
    Article
  8. Accurate RNA consensus sequencing for high-fidelity detection of transcriptional mutagenesis-induced epimutations.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  9. Evaluation of in vivo mutagenesis for assessing the health risk of air pollutants.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2017
    Review
  10. Article
  11. Why Cockayne syndrome patients do not get cancer despite their DNA repair deficiency.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  12. Article
  13. Article
  14. Article
  15. Article
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  18. Article
  19. Review
  20. A switch between DNA polymerases δ and λ promotes error-free bypass of 8-oxo-G lesions.Proceedings of the National Academy of Sciences of the United States of America · 2012
    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

2 authors at 2 institutions in 1 country.

Dong-Hyun LeeDivision of Biology, Beckman Research Institute of the City of Hope, Duarte, CA 91010, United States.
Gerd P Pfeifer
Beckman Research InstituteCity of Hope · US

Funding

UV damage, repair, and mutagenesisR37ES006070 · NIEHS · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI PFEIFER, GERD P · 2004 to 2013
$3.7M
UV DAMAGE, REPAIR AND MUTAGENESISR01ES006070 · NIEHS · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI PFEIFER, GERD P · 1992 to 2003
$1.1M
NIEHS NIH HHS ES06070NIEHS NIH HHS R01 ES006070NIEHS NIH HHS R37 ES006070
6 · The paper itself

Abstract

7,8-Dihydro-8-oxo-2'-deoxyguanosine (8-oxo-dG) is one of the most common DNA lesions induced by oxidative stress. This lesion can be bypassed by DNA polymerase eta (Pol eta) using in vitro translesion synthesis (TLS) reactions. However, the role that Pol eta plays in vivo contributing to 8-oxo-dG mutagenesis remains unclear. To clarify the role of Pol eta in 8-oxo-dG mutagenesis, we have used an siRNA knockdown approach in combination with a supF shuttle vector (pSP189) which replicates in mammalian cells. The pSP189 plasmid was treated with methylene blue plus light (MBL), which produces predominantly 8-oxo-dG in DNA, and was then replicated in GM637 cells in presence of siRNA that knocks down the expression of Pol eta, or in XP-V cells, which lack functional Pol eta. The mutant frequencies were increased in the Pol eta siRNA knockdown cells and in XP-V cells relative to control, meaning that Pol eta plays an important role in preventing 8-oxo-dG mutagenesis. In the same system, knockdown of OGG1 also led to an increase in mutagenesis. Neither the type of mutations nor their distribution along the supF gene were significantly different between control and target specific siRNA-transfected cells (or XP-V cells) and were predominantly G to T transversions. These results show that Pol eta has an important role in error-free 8-oxo-dG lesion bypass and avoidance of oxidative stress-induced mutagenesis in vivo.

Indexed as

DNA DamageMutagenesis8-Hydroxy-2'-DeoxyguanosineBase SequenceBlotting, WesternCells, CulturedDeoxyguanosineDNADNA-Directed DNA PolymeraseDNA GlycosylasesDNA RepairDNA ReplicationEscherichia coliEscherichia coli ProteinsFibroblastsGenetic Vectors8-Hydroxy-2'-DeoxyguanosineDeoxyguanosineDNADNA-Directed DNA PolymeraseDNA GlycosylasesEscherichia coli ProteinsMethylene BlueNucleic Acid Synthesis Inhibitorsoxoguanine glycosylase 1, humanRad30 proteinRNA, Small InterferingY-Family DNA Polymerases

Identifiers

PMID18359049
PMCPMC2410043
OpenAlexW2076924472

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.