ArticleNucleic acids research2012
Structure and stability of DNA containing an aristolactam II-dA lesion: implications for the NER recognition of bulky adducts.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 46 citations in OpenAlex.
- Article
- Aristolochic acid-associated cancers: a public health risk in need of global action.Nature reviews. Cancer · 2022Review
- Role of Base Excision Repair Pathway in the Processing of Complex DNA Damage Generated by Oxidative Stress and Anticancer Drugs.Frontiers in cell and developmental biology · 2020Review
- Systematic Overview of Aristolochic Acids: Nephrotoxicity, Carcinogenicity, and Underlying Mechanisms.Frontiers in pharmacology · 2019Review
- Worldwide research trends on aristolochic acids (1957-2017): Suggestions for researchers.PloS one · 2019Article
- Molecular basis for damage recognition and verification by XPC-RAD23B and TFIIH in nucleotide excision repair.DNA repair · 2018Review
- Repair-Resistant DNA Lesions.Chemical research in toxicology · 2017Review
- Effect of base sequence context on the conformational heterogeneity of aristolactam-I adducted DNA: structural and energetic insights into sequence-dependent repair and mutagenicity.Toxicology research · 2016Article
- Adenine versus guanine DNA adducts of aristolochic acids: role of the carcinogen-purine linkage in the differential global genomic repair propensity.Nucleic acids research · 2015Article
- DNA Sequence Modulates Geometrical Isomerism of the trans-8,9- Dihydro-8-(2,6-diamino-4-oxo-3,4-dihydropyrimid-5-yl-formamido)- 9-hydroxy Aflatoxin B1 Adduct.Chemical research in toxicology · 2015Article
- Adenine-DNA adduct derived from the nitroreduction of 6-nitrochrysene is more resistant to nucleotide excision repair than guanine-DNA adducts.Chemical research in toxicology · 2013Article
- Free energy profiles of base flipping in intercalative polycyclic aromatic hydrocarbon-damaged DNA duplexes: energetic and structural relationships to nucleotide excision repair susceptibility.Chemical research in toxicology · 2013Article
- Adenine-DNA adducts derived from the highly tumorigenic Dibenzo[a,l]pyrene are resistant to nucleotide excision repair while guanine adducts are not.Chemical research in toxicology · 2013Article
- Article
- The efficiencies of damage recognition and excision correlate with duplex destabilization induced by acetylaminofluorene adducts in human nucleotide excision repair.Chemical research in toxicology · 2012Article
- Structure and stability of duplex DNA containing (5'S)-5',8-cyclo-2'-deoxyadenosine: an oxidatively generated lesion repaired by NER.Chemical research in toxicology · 2012Article
- Aristolochic acid-associated urothelial cancer in Taiwan.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Nucleotide excision repair efficiencies of bulky carcinogen-DNA adducts are governed by a balance between stabilizing and destabilizing interactions.Biochemistry · 2012Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Aristolochic acids I and II are prevalent plant toxicants found in the Aristolochiaceae plant family. Metabolic activation of the aristolochic acids leads to the formation of a cyclic N-hydroxylactam product that can react with the peripheral amino group of purine bases generating bulky DNA adducts. These lesions are mutagenic and established human carcinogens. Interestingly, although AL-dG adducts progressively disappear from the DNA of laboratory animals, AL-dA lesions has lasting persistence in the genome. We describe here NMR structural studies of an undecameric duplex damaged at its center by the presence of an ALII-dA adduct. Our data establish a locally perturbed double helical structure that accommodates the bulky adduct by displacing the counter residue into the major groove and stacking the ALII moiety between flanking bases. The presence of the ALII-dA perturbs the conformation of the 5'-side flanking base pair, but all other pairs of the duplex adopt standard conformations. Thermodynamic studies reveal that the lesion slightly decreases the energy of duplex formation in a sequence-dependent manner. We discuss our results in terms of its implications for the repair of ALII-dA adducts in mammalian cells.
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