ArticleThe EMBO journal2001
Unique misinsertion specificity of poliota may decrease the mutagenic potential of deaminated cytosines.
Article in The EMBO journal, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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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.
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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
47 citing papers in PubMed.
- 8-Oxoguanine: A Lesion, an Epigenetic Mark, or a Molecular Signal?International journal of molecular sciences · 2025Review
- RNA Editing of the Human DNA Glycosylase NEIL1 Alters Its Removal of 5-Hydroxyuracil Lesions in DNA.Biochemistry · 2021Article
- DNA Damage Tolerance Pathways in Human Cells: A Potential Therapeutic Target.Frontiers in oncology · 2021Review
- Mysterious and fascinating: DNA polymerase ɩ remains enigmatic 20 years after its discovery.DNA repair · 2020Review
- Three Human Pol ι Variants with Impaired Polymerase Activity Fail to Rescue HChemical research in toxicology · 2020Article
- Biochemical reconstitution of UV-induced mutational processes.Nucleic acids research · 2019Article
- Deoxyuridine in DNA has an inhibitory and promutagenic effect on RNA transcription by diverse RNA polymerases.Nucleic acids research · 2019Article
- Review
- Translesion DNA polymerases in eukaryotes: what makes them tick?Critical reviews in biochemistry and molecular biology · 2017Review
- Breaking bad: The mutagenic effect of DNA repair.DNA repair · 2015Review
- Minimal detection of nuclear mutations in XP-V and normal cells treated with oxidative stress inducing agents.Journal of biochemical and molecular toxicology · 2014Article
- The Werner syndrome protein limits the error-prone 8-oxo-dG lesion bypass activity of human DNA polymerase kappa.Nucleic acids research · 2014Article
- Replication across regioisomeric ethylated thymidine lesions by purified DNA polymerases.Chemical research in toxicology · 2013Article
- MUTYH DNA glycosylase: the rationale for removing undamaged bases from the DNA.Frontiers in genetics · 2013Article
- Pathways for repairing and tolerating the spectrum of oxidative DNA lesions.Cancer letters · 2012Review
- Thermodynamic signature of DNA damage: characterization of DNA with a 5-hydroxy-2'-deoxycytidine·2'-deoxyguanosine base pair.Biochemistry · 2012Article
- Y-family DNA polymerases and their role in tolerance of cellular DNA damage.Nature reviews. Molecular cell biology · 2012Review
- Translesion DNA polymerases and cancer.Frontiers in genetics · 2012Article
- The miscoding potential of 5-hydroxycytosine arises due to template instability in the replicative polymerase active site.Biochemistry · 2011Article
- Poli: Shining light on repair of oxidative DNA lesions and mutations.Cell cycle (Georgetown, Tex.) · 2011Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
DNA polymerase iota (poliota) is a distributive error-prone enzyme that can incorporate nucleotides opposite a variety of DNA lesions. Further elongation is, however, either substantially inhibited or completely abolished. Here, we provide evidence that poliota can facilitate the efficient bypass of uracil and its derivatives as well as oxidized cytosine and guanine residues. The fidelity of translesion replication depends upon the lesion encountered. Correct nucleotides were inserted preferentially opposite 7,8-dihydro-8-oxoguanine (8-oxoG) and 5-hydroxycytosine (5-OHC). However, when bypassing uracil, 5-hydroxyuracil (5-OHU) or 5,6-dihydrouracil (5,6-DHU), poliota inserted T and G with a 4- to 26-fold preference over the Watson-Crick base, A. While the T:U, T:5-OHU and T:5,6-DHU mispairs were extended poorly, the G:U, G:5-OHU and G:5,6-DHU mispairs were extended with equal or greater efficiency than the correctly paired primer termini. Thus, poliota-dependent misinsertion of G opposite uracil and its derivatives may actually provide a mechanism whereby mammalian cells can decrease the mutagenic potential of lesions formed via the deamination of cytosine.
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