ArticleThe Journal of biological chemistry2014
Error-prone replication bypass of the primary aflatoxin B1 DNA adduct, AFB1-N7-Gua.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 63 citations in OpenAlex.
- Redox-sensitive and inflammatory pathway modulation by Chrysin confers protection against aflatoxin B1-induced hepato-renal damage.Mycotoxin research · 2026Article
- Aflatoxin B1 and food safety: Mechanisms of action associated to Hepatocellular Carcinoma.Archives of microbiology · 2026Review
- The adduct models of aflatoxins with DNA and effects on DNA polymerase Ⅳ.Journal of molecular modeling · 2026Article
- Integrative transcriptomic and machine learning framework reveals candidate genes and potential mechanisms of aflatoxin B1 exposure in breast cancer.Scientific reports · 2026Article
- Surfactant protein D: prognostic insights and emerging therapeutic roles in cancer.Frontiers in immunology · 2026Review
- Mycotoxin Contamination: Occurrence, Biotransformation, Pathogenic Mechanisms, and Strategies for Nutritional Intervention.Molecules (Basel, Switzerland) · 2025Review
- Aflatoxin BEnvironmental and molecular mutagenesis · 2025Article
- Role of NEIL1 in genome maintenance.DNA repair · 2025Review
- Aflatoxin BEnvironmental toxicology and pharmacology · 2025Article
- Structurally Similar Mycotoxins Aflatoxin BToxins · 2025Article
- Nucleotide excision repair of aflatoxin-induced DNA damage within the 3D human genome organization.Nucleic acids research · 2024Article
- Functional characterization of single nucleotide polymorphic variants of DNA repair enzyme NEIL1 in South Asian populations.DNA repair · 2024Article
- The Novel Role of the NLRP3 Inflammasome in Mycotoxin-Induced Toxicological Mechanisms.Veterinary sciences · 2024Review
- Frequencies and spectra of aflatoxin BNAR molecular medicine · 2024Article
- Synthesis and Characterization ofACS omega · 2023Article
- Overview of Adductomics in Toxicology.Current protocols · 2023Article
- Mycotoxin source and its exposure causing mycotoxicoses.Bioinformation · 2023Review
- Construction of a Novel LncRNA Signature Related to Genomic Instability to Predict the Prognosis and Immune Activity of Patients With Hepatocellular Carcinoma.Frontiers in immunology · 2022Article
- New Insights Into the Persistent Effects of Acute Exposure to AFBFrontiers in microbiology · 2022Article
- Resveratrol Relieved Acute Liver Damage in Ducks (Animals : an open access journal from MDPI · 2021Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Hepatocellular carcinomas (HCCs) are the third leading cause of cancer deaths worldwide. The highest rates of early onset HCCs occur in geographical regions with high aflatoxin B1 (AFB1) exposure, concomitant with hepatitis B infection. Although the carcinogenic basis of AFB1 has been ascribed to its mutagenic effects, the mutagenic property of the primary AFB1-DNA adduct, AFB1-N7-Gua, in mammalian cells has not been studied extensively. Taking advantage of the ability to create vectors containing a site-specific DNA adduct, the mutagenic potential was determined in primate cells. This adduct was highly mutagenic following replication in COS-7 cells, with a mutation frequency of 45%. The spectrum of mutations was predominantly G to T base substitutions, a result that is consistent with previous mutation data derived from aflatoxin-associated HCCs. To assess which DNA polymerases (pol) might contribute to the mutational outcome, in vitro replication studies were performed. Unexpectedly, replicative pol δ and the error-prone translesion synthesis pol ζ were able to accurately bypass AFB1-N7-Gua. In contrast, replication bypass using pol κ was shown to occur with low fidelity and could account for the commonly detected G to T transversions.
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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.