ArticleNucleic acids research2003
Human RNA polymerase II is partially blocked by DNA adducts derived from tumorigenic benzo[c]phenanthrene diol epoxides: relating biological consequences to conformational preferences.
Article in Nucleic acids research, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Molecular mechanisms of air pollution-induced carcinogenesis and the emerging role of microplastics.Human genomics · 2025Review
- Keep calm and reboot - how cells restart transcription after DNA damage and DNA repair.FEBS letters · 2025Review
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Quantitative analysis of PAH compounds in DWH crude oil and their effects on Caenorhabditis elegans germ cell apoptosis, associated with CYP450s upregulation.The Science of the total environment · 2020Article
- The DNA damage response to transcription stress.Nature reviews. Molecular cell biology · 2019Review
- Nucleotide Excision Repair and Transcription-coupled DNA Repair Abrogate the Impact of DNA Damage on Transcription.The Journal of biological chemistry · 2016Article
- Transcription Blockage Leads to New Beginnings.Biomolecules · 2015Review
- RNA polymerase II transcriptional fidelity control and its functional interplay with DNA modifications.Critical reviews in biochemistry and molecular biology · 2015Review
- An in vitro method for detecting genetic toxicity based on inhibition of RNA synthesis by DNA lesions.Genes and environment : the official journal of the Japanese Environmental Mutagen Society · 2015Article
- Molecular basis of transcriptional fidelity and DNA lesion-induced transcriptional mutagenesis.DNA repair · 2014Review
- Effect of a monofunctional phenanthriplatin-DNA adduct on RNA polymerase II transcriptional fidelity and translesion synthesis.Journal of the American Chemical Society · 2013Article
- Transcription elongation past O6-methylguanine by human RNA polymerase II and bacteriophage T7 RNA polymerase.Nucleic acids research · 2008Article
- Transcription of DNA containing the 5-guanidino-4-nitroimidazole lesion by human RNA polymerase II and bacteriophage T7 RNA polymerase.DNA repair · 2008Article
- Transcription processing at 1,N2-ethenoguanine by human RNA polymerase II and bacteriophage T7 RNA polymerase.Journal of molecular biology · 2008Article
- The role of polycyclic aromatic hydrocarbon-DNA adducts in inducing mutations in mouse skin.Mutation research · 2008Article
- Malondialdehyde adducts in DNA arrest transcription by T7 RNA polymerase and mammalian RNA polymerase II.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Environmental polycyclic aromatic hydrocarbons (PAHs) are metabolically activated to diol epoxides that can react with DNA, resulting in covalent modifications to the bases. The (+)- and (-)-3,4-dihydroxy-1,2-epoxy-1,2,3,4-tetrahydro-benzo[c]phenanthrene (anti-BPhDE) isomers are diol epoxide metabolites of the PAH benzo[c]phenanthrene (BPh). These enantiomers readily react with DNA at the N6 position of adenine, forming bulky (+)-1R- or (-)-1S-trans-anti-[BPh]-N6-dA adducts. Transcription-coupled nucleotide excision repair clears such bulky adducts from cellular DNA, presumably in response to RNA polymerase transcription complexes that stall at the bulky lesions. Little is known about the effects of [BPh]-N6-dA lesions on RNA polymerase II, hence, the behavior of human RNA polymerase II was examined at these adducts. A site-specific, stereochemically pure [BPh]-N6-dA adduct was positioned on the transcribed or non-transcribed strand of a DNA template with a suitable promoter for RNA polymerase II located upstream from the lesion. Transcription reactions were then carried out with HeLa nuclear extract. Each [BPh]-dA isomer strongly impeded human RNA polymerase II progression when it was located on the transcribed strand; however, a small but significant degree of lesion bypass occurred, and the extent of polymerase blockage and bypass was dependent on the stereochemistry of the adduct. Molecular modeling of the lesions supports the idea that each adduct can exist in two orientations within the polymerase active site, one that permits nucleotide incorporation and another that blocks the RNA polymerase nucleotide entry channel, thus preventing base incorporation and causing the polymerase to stall or arrest.
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Registered trials
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