ArticleNucleic acids research2010
O6-methylguanine induces altered proteins at the level of transcription in human cells.
Article in Nucleic acids research, 2010. 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, 43 citations in OpenAlex.
- Assessment and detection of nucleotide excision repair capability in human cells: a critical review of current functional methods.Molecular biology reports · 2026Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Transcription blocking properties and transcription-coupled repair of NThe Journal of biological chemistry · 2025Article
- Proteins Associated with Neurodegenerative Diseases: Link to DNA Repair.Biomedicines · 2024Review
- Labeling and sequencing nucleic acid modifications using bio-orthogonal tools.RSC chemical biology · 2022Review
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Large-scale preparation of fluorescence multiplex host cell reactivation (FM-HCR) reporters.Nature protocols · 2021Article
- The complexity and regulation of repair of alkylation damage to nucleic acids.Critical reviews in biochemistry and molecular biology · 2021Review
- EmPC-seq: Accurate RNA-sequencing and Bioinformatics Platform to Map RNA Polymerases and Remove Background Error.Bio-protocol · 2021Article
- Transcriptional mutagenesis dramatically alters genome-wide p53 transactivation landscape.Scientific reports · 2020Article
- EGFP Reporters for Direct and Sensitive Detection of Mutagenic Bypass of DNA Lesions.Biomolecules · 2020Article
- The roles of polymerases ν and θ in replicative bypass ofThe Journal of biological chemistry · 2020Article
- Gre-family factors modulate DNA damage sensing byRNA biology · 2019Article
- Cytotoxic and Mutagenic Properties of C1' and C3'-Epimeric Lesions of 2'-Deoxyribonucleosides in Human Cells.ACS chemical biology · 2019Article
- Cytotoxic and mutagenic properties of minor-grooveThe Journal of biological chemistry · 2018Article
- Article
- Mechanism of RNA polymerase II stalling by DNA alkylation.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Position-dependent effects of regioisomeric methylated adenine and guanine ribonucleosides on translation.Nucleic acids research · 2017Article
- 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 · 2017Article
- 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
O(6)-Methylguanine (O(6)-meG), which is produced in DNA following exposure to methylating agents, instructs human RNA polymerase II to mis-insert bases opposite the lesion during transcription. In this study, we examined the effect of O(6)-meG on transcription in human cells and investigated the subsequent effects on protein function following translation of the resulting mRNA. In HEK293 cells, O(6)-meG induced incorporation of uridine or cytidine in nascent RNA opposite the adduct. In cells containing active O(6)-alkylguanine-DNA alkyltransferase (AGT), which repairs O(6)-meG, 3% misincorporation of uridine was observed opposite the lesion. In cells where AGT function was compromised by addition of the AGT inhibitor O(6)-benzylguanine, ∼ 58% of the transcripts contained a uridine misincorporation opposite the lesion. Furthermore, the altered mRNA induced changes to protein function as demonstrated through recovery of functional red fluorescent protein (RFP) from DNA coding for a non-fluorescent variant of RFP. These data show that O(6)-meG is highly mutagenic at the level of transcription in human cells, leading to an altered protein load, especially when AGT is inhibited.
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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.