ArticleJournal of nucleic acids2010
Aflatoxin B(1)-Associated DNA Adducts Stall S Phase and Stimulate Rad51 foci in Saccharomyces cerevisiae.
Article in Journal of nucleic acids, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- High-throughput screening of the Saccharomyces cerevisiae genome for 2-amino-3-methylimidazo [4,5-f] quinoline resistance identifies colon cancer-associated genes.G3 (Bethesda, Md.) · 2023Article
- Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020Article
- tRNA modification and cancer: potential for therapeutic prevention and intervention.Future medicinal chemistry · 2019Review
- TheFrontiers in microbiology · 2019Review
- An in vitro system for measuring genotoxicity mediated by human CYP3A4 in Saccharomyces cerevisiae.Environmental and molecular mutagenesis · 2017Article
- CYP1A1 I462V polymorphism is associated with reduced genotoxicity in yeast despite positive association with increased cancer risk.Mutation research. Genetic toxicology and environmental mutagenesis · 2017Article
- Activation of aflatoxin B1 by expression of human CYP1A2 polymorphisms in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesis · 2014Article
- CYP1B1 converts procarcinogens into genotoxins in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesisArticle
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
Abstract
AFB(1) is a potent recombinagen in budding yeast. AFB(1) exposure induces RAD51 expression and triggers Rad53 activation in yeast cells that express human CYP1A2. It was unknown, however, when and if Rad51 foci appear. Herein, we show that Rad53 activation correlates with cell-cycle delay in yeast and the subsequent formation of Rad51 foci. In contrast to cells exposed to X-rays, in which Rad51 foci appear exclusively in G2 cells, Rad51 foci in AFB(1)-exposed cells can appear as soon as cells enter S phase. Although rad51 and rad4 mutants are mildly sensitive to AFB(1), chronic exposure of the NER deficient rad4 cells to AFB(1) leads to increased lag times, while rad4 rad51 double mutants exhibit synergistic sensitivity and do not grow when exposed to 50 μM AFB(1). We suggest RAD51 functions to facilitate DNA replication after replication fork stalling or collapse in AFB(1)-exposed cells.
Identifiers
What OpenQuestion holds
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.