ArticleNucleic acids research2012
Lack of recognition by global-genome nucleotide excision repair accounts for the high mutagenicity and persistence of aristolactam-DNA 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 59 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
59 citing papers in PubMed, 106 citations in OpenAlex.
- Click-code-seq reveals strand biases of DNA oxidation and depurination in human genome.Nature chemical biology · 2026Article
- Matricellular protein SMOC2 safeguards tubular integrity in acute kidney injury via integrin β3-dependent inhibition of CCND1-CDK4/6 axis.Molecular biomedicine · 2026Article
- Whether aristolochic acid directly drives hepatocarcinogenesis: comprehensive investigations from mutational signatures to animal models.Archives of toxicology · 2025Review
- Transcription-Coupled Nucleotide Excision Repair: A Faster Solution or the Only Option?Biomolecules · 2025Review
- Mechanisms of DNA repair and mutagenesis induced by acetaldehyde, acrolein, aristolochic acids, and vinyl chloride.Journal of environmental science and health. Part C, Toxicology and carcinogenesis · 2025Review
- Article
- Cholangiocarcinoma: Recent Advances in Molecular Pathobiology and Therapeutic Approaches.Cancers · 2024Review
- SGLT2 inhibitor dapagliflozin protects the kidney in a murine model of Balkan nephropathy.American journal of physiology. Renal physiology · 2024Article
- Pathological consequences of DNA damage in the kidney.Nature reviews. Nephrology · 2023Review
- Aristolochic acid-associated cancers: a public health risk in need of global action.Nature reviews. Cancer · 2022Review
- Transcriptional Perturbations of 2,6-Diaminopurine and 2-Aminopurine.ACS chemical biology · 2022Article
- Aristolochic acids exposure was not the main cause of liver tumorigenesis in adulthood.Acta pharmaceutica Sinica. B · 2022Article
- Aristolochic acid IVa forms DNA adducts in vitro but is non-genotoxic in vivo.Archives of toxicology · 2021Article
- Krüppel-like factor 6-mediated loss of BCAA catabolism contributes to kidney injury in mice and humans.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Comparative Research of Chemical Profiling in Different Parts ofMolecules (Basel, Switzerland) · 2021Article
- Aristolochic acid-associated urinary tract cancers: an updated meta-analysis of risk and oncologic outcomes after surgery and systematic review of molecular alterations observed in human studies.Therapeutic advances in drug safety · 2021Article
- The DNA damage-sensing NER repair factor XPC-RAD23B does not recognize bulky DNA lesions with a missing nucleotide opposite the lesion.DNA repair · 2020Article
- Defining in vivo dose-response curves for kidney DNA adduct formation of aristolochic acid I in rat, mouse and human by an in vitro and physiologically based kinetic modeling approach.Journal of applied toxicology : JAT · 2020Article
- Clinicopathologic characteristics and prognosis of upper tract urothelial carcinoma complicated with aristolochic acid nephropathy after radical nephroureterectomy.BMC complementary medicine and therapies · 2020Article
- Mutational signatures are jointly shaped by DNA damage and repair.Nature communications · 2020Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Exposure to aristolochic acid (AA), a component of Aristolochia plants used in herbal remedies, is associated with chronic kidney disease and urothelial carcinomas of the upper urinary tract. Following metabolic activation, AA reacts with dA and dG residues in DNA to form aristolactam (AL)-DNA adducts. These mutagenic lesions generate a unique TP53 mutation spectrum, dominated by A:T to T:A transversions with mutations at dA residues located almost exclusively on the non-transcribed strand. We determined the level of AL-dA adducts in human fibroblasts treated with AA to determine if this marked strand bias could be accounted for by selective resistance to global-genome nucleotide excision repair (GG-NER). AL-dA adduct levels were elevated in cells deficient in GG-NER and transcription-coupled NER, but not in XPC cell lines lacking GG-NER only. In vitro, plasmids containing a single AL-dA adduct were resistant to the early recognition and incision steps of NER. Additionally, the NER damage sensor, XPC-RAD23B, failed to specifically bind to AL-DNA adducts. However, placing AL-dA in mismatched sequences promotes XPC-RAD23B binding and renders this adduct susceptible to NER, suggesting that specific structural features of this adduct prevent processing by NER. We conclude that AL-dA adducts are not recognized by GG-NER, explaining their high mutagenicity and persistence in target tissues.
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