ArticlePLoS genetics2013
In vivo bypass of 8-oxodG.
Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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.
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Who cites it
25 citing papers in PubMed, 34 citations in OpenAlex.
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisNAR cancer · 2026Article
- Nucleotide salvage, genome instability, and potential therapeutic applications.Nucleic acids research · 2026Review
- Differential roles of Rad18 in repressing carcinogen- and oncogene-driven mutagenesisbioRxiv : the preprint server for biology · 2025Article
- E-Cigarette effects on oral health: A molecular perspective.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2025Review
- 8-Oxoadenine: A «New» Player of the Oxidative Stress in Mammals?International journal of molecular sciences · 2024Review
- Transient State Kinetics ofBiochemistry · 2022Article
- Genome-Wide Analysis of Cadmium-Induced, Germline Mutations in a Long-TermEnvironmental health perspectives · 2021Article
- Genetic Control of Oxidative Mutagenesis inJournal of bacteriology · 2020Article
- Mutagenesis mechanism of the major oxidative adenine lesion 7,8-dihydro-8-oxoadenine.Nucleic acids research · 2020Article
- Mutagenic Replication of the Major Oxidative Adenine Lesion 7,8-Dihydro-8-oxoadenine by Human DNA Polymerases.Journal of the American Chemical Society · 2019Article
- DNA polymerase η contributes to genome-wide lagging strand synthesis.Nucleic acids research · 2019Article
- Review
- Oxidized Cell-Free DNA Role in the Antioxidant Defense Mechanisms under Stress.Oxidative medicine and cellular longevity · 2019Article
- The Translesion Polymerase Pol η Is Required for Efficient Epstein-Barr Virus Infectivity and Is Regulated by the Viral Deubiquitinating Enzyme BPLF1.Journal of virology · 2017Article
- A 'Semi-Protected Oligonucleotide Recombination' Assay for DNA Mismatch Repair in vivo Suggests Different Modes of Repair for Lagging Strand Mismatches.Nucleic acids research · 2017Article
- Translesion Synthesis of 2'-Deoxyguanosine Lesions by Eukaryotic DNA Polymerases.Chemical research in toxicology · 2017Article
- Impact of Ribonucleotide Backbone on Translesion Synthesis and Repair of 7,8-Dihydro-8-oxoguanine.The Journal of biological chemistry · 2016Article
- Non-canonical actions of mismatch repair.DNA repair · 2016Review
- Article
- Replicative DNA polymerase δ but not ε proofreads errors in Cis and in Trans.PLoS genetics · 2015Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
8-oxoG is one of the most common and mutagenic DNA base lesions caused by oxidative damage. However, it has not been possible to study the replication of a known 8-oxoG base in vivo in order to determine the accuracy of its replication, the influence of various components on that accuracy, and the extent to which an 8-oxoG might present a barrier to replication. We have been able to place a single 8-oxoG into the Saccharomyces cerevisiae chromosome in a defined location using single-strand oligonucleotide transformation and to study its replication in a fully normal chromosome context. During replication, 8-oxoG is recognized as a lesion and triggers a switch to translesion synthesis by Pol η, which replicates 8-oxoG with an accuracy (insertion of a C opposite the 8-oxoG) of approximately 94%. In the absence of Pol η, template switching to the newly synthesized sister chromatid is observed at least one third of the time; replication of the 8-oxoG in the absence of Pol η is less than 40% accurate. The mismatch repair (MMR) system plays an important role in 8-oxoG replication. Template switching is blocked by MMR and replication accuracy even in the absence of Pol η is approximately 95% when MMR is active. These findings indicate that in light of the overlapping mechanisms by which errors in 8-oxoG replication can be avoided in the cell, the mutagenic threat of 8-oxoG is due more to its abundance than the effect of a single lesion. In addition, the methods used here should be applicable to the study of any lesion that can be stably incorporated into synthetic oligonucleotides.
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Registered trials
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.