ArticleThe Journal of biological chemistry2011
The roles of DNA polymerases κ and ι in the error-free bypass of N2-carboxyalkyl-2'-deoxyguanosine lesions in mammalian cells.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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Who cites it
36 citing papers in PubMed, 50 citations in OpenAlex.
- Nucleotide salvage, genome instability, and potential therapeutic applications.Nucleic acids research · 2026Review
- Tissue-specific mutagenesis from endogenous guanine damage is suppressed by Polκ and DNA repair.Nature communications · 2025Article
- HMGB3 and SUB1 Bind to and Facilitate the Repair ofJournal of the American Chemical Society · 2024Article
- LC-MS/MS for Assessing the Incorporation and Repair ofChemical research in toxicology · 2022Article
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- DNA Polymerase η Promotes the Transcriptional Bypass ofJournal of the American Chemical Society · 2021Article
- The roles of polymerases ν and θ in replicative bypass ofThe Journal of biological chemistry · 2020Article
- The Impact of Minor-GrooveACS chemical biology · 2019Article
- Biological Evaluation of DNA Biomarkers in a Chemically Defined and Site-Specific Manner.Toxics · 2019Review
- DNA replication studies ofThe Journal of biological chemistry · 2019Article
- Translesion Synthesis DNA Polymerase Kappa Is Indispensable for DNA Repair Synthesis in Cisplatin Exposed Dorsal Root Ganglion Neurons.Molecular neurobiology · 2018Article
- Mechanism of DNA alkylation-induced transcriptional stalling, lesion bypass, and mutagenesis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Replication and repair of a reduced 2΄-deoxyguanosine-abasic site interstrand cross-link in human cells.Nucleic acids research · 2017Article
- Mouse DNA polymerase ι lacking the forty-two amino acids encoded by exon-2 is catalytically inactive in vitro.DNA repair · 2017Article
- Mass Spectrometry-Based Quantitative Strategies for Assessing the Biological Consequences and Repair of DNA Adducts.Accounts of chemical research · 2016Review
- Mass spectrometry for the assessment of the occurrence and biological consequences of DNA adducts.Chemical Society reviews · 2015Review
- Posttranslational Regulation of Human DNA Polymerase ι.The Journal of biological chemistry · 2015Article
- Transcriptional inhibition and mutagenesis induced by N-nitroso compound-derived carboxymethylated thymidine adducts in DNA.Nucleic acids research · 2015Article
- Roles of PCNA ubiquitination and TLS polymerases κ and η in the bypass of methyl methanesulfonate-induced DNA damage.Nucleic acids research · 2015Article
- Transcriptional bypass of regioisomeric ethylated thymidine lesions by T7 RNA polymerase and human RNA polymerase II.Nucleic acids research · 2014Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
To counteract the deleterious effects of DNA damage, cells are equipped with specialized polymerases to bypass DNA lesions. Previous biochemical studies revealed that DinB family DNA polymerases, including Escherichia coli DNA polymerase IV and human DNA polymerase κ, efficiently incorporate the correct nucleotide opposite some N(2)-modified 2'-deoxyguanosine derivatives. Herein, we used shuttle vector technology and demonstrated that deficiency in Polk or Poli in mouse embryonic fibroblast (MEF) cells resulted in elevated frequencies of G→T and G→A mutations at N(2)-(1-carboxyethyl)-2'-deoxyguanosine (N(2)-CEdG) and N(2)-carboxymethyl-2'-deoxyguanosine (N(2)-CMdG) sites. Steady-state kinetic measurements revealed that human DNA polymerase ι preferentially inserts the correct nucleotide, dCMP, opposite N(2)-CEdG lesions. In contrast, no mutation was found after the N(2)-CEdG- and N(2)-CMdG-bearing plasmids were replicated in POLH-deficient human cells or Rev3-deficient MEF cells. Together, our results revealed that, in mammalian cells, both polymerases κ and ι are necessary for the error-free bypass of N(2)-CEdG and N(2)-CMdG. However, in the absence of polymerase κ or ι, other translesion synthesis polymerase(s) could incorporate nucleotide(s) opposite these lesions but would do so inaccurately.
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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.