ArticleProceedings of the National Academy of Sciences of the United States of America2004
Malondialdehyde adducts in DNA arrest transcription by T7 RNA polymerase and mammalian RNA polymerase II.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 71 citations in OpenAlex.
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- Aldo-keto reductase 1B10 as a Carcinogenic but Not a Prognostic Factor in Colorectal Cancer.Journal of Cancer · 2024Article
- RNA polymerase pausing, stalling and bypass during transcription of damaged DNA: from molecular basis to functional consequences.Nucleic acids research · 2022Review
- Transcriptional Bypass of DNA-Protein and DNA-Peptide Conjugates by T7 RNA Polymerase.ACS chemical biology · 2019Article
- Obesity and cancer: A mechanistic overview of metabolic changes in obesity that impact genetic instability.Molecular carcinogenesis · 2019Review
- Pathogenesis and treatment of autoimmune rheumatic diseases.Current opinion in rheumatology · 2019Review
- 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
- The Nonbulky DNA Lesions Spiroiminodihydantoin and 5-Guanidinohydantoin Significantly Block Human RNA Polymerase II Elongation in Vitro.Biochemistry · 2017Article
- A novel role for transcription-coupled nucleotide excision repair for the in vivo repair of 3,N4-ethenocytosine.Nucleic acids research · 2017Article
- RNA polymerase II senses obstruction in the DNA minor groove via a conserved sensor motif.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Oxidative Stress and Carbonyl Lesions in Ulcerative Colitis and Associated Colorectal Cancer.Oxidative medicine and cellular longevity · 2016Review
- 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
- Molecular basis of transcriptional fidelity and DNA lesion-induced transcriptional mutagenesis.DNA repair · 2014Review
- Metabolic control of the epigenome in systemic Lupus erythematosus.Autoimmunity · 2014Review
- The link between intraneuronal N-truncated amyloid-β peptide and oxidatively modified lipids in idiopathic autism and dup(15q11.2-q13)/autism.Acta neuropathologica communications · 2013Article
- Article
- Can apricot kernels fatty acids delay the atrophied hepatocytes from progression to fibrosis in dimethylnitrosamine (DMN)-induced liver injury in rats?Lipids in health and disease · 2011Article
- DNA repair deficiency in neurodegeneration.Progress in neurobiology · 2011Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Malondialdehyde, a genotoxic byproduct of lipid peroxidation, reacts with guanine in DNA to form pyrimido[1,2-alpha]purin-10(3H)one (M(1)dG), the first endogenous DNA lesion found to be a target of nucleotide excision repair enzymes. A subpathway of nucleotide excision repair, transcription-coupled repair, is thought to occur when RNA polymerase (RNAP) is arrested at damage in transcribed DNA strands and might function for efficient removal of M(1)dG in active genes. Results presented here show that M(1)dG and its stable, exocyclic analog 1,N(2)-propanodeoxyguanine (PdG), arrest translocation of T7 RNAP and mammalian RNAPII when located in the transcribed strand of a DNA template. M(1)dG paired with thymine is exocyclic and poses a stronger block to transcription than the acyclic N(2)-(3-oxo-1-propenyl)-dG, formed upon cytosine-catalyzed opening of M(1)dG in duplex DNA. PdG is a complete block to RNAPII regardless of base pairing. The elongation factor TFIIS (SII) induces reversal and RNA transcript cleavage by RNAPII arrested at PdG. Thus, arrested RNAPII complexes may be stable at M(1)dG in cells and may resume transcription once the offending adduct is removed. The conclusion from this work is that malondialdehyde adducts in the transcribed strand of expressed genes are strong blocks to RNAPs and are targets for cellular transcription-coupled repair. If so, then M(1)dG, already known to be highly mutagenic in human cells, also may contribute to apoptosis in the developing tissues of individuals with Cockayne's syndrome, a hereditary disorder characterized by transcription-coupled repair deficiency.
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