Evidence map›Paper›PMID 15988000›Full record

ArticleMolecular and cellular biology2005

Expression of a human cytochrome p450 in yeast permits analysis of pathways for response to and repair of aflatoxin-induced DNA damage.

Yingying Guo, Linda L Breeden, Helmut Zarbl, Bradley D Preston, David L Eaton

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.9field-weighted citation impact, top 28% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

11 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. FeFood chemistry. Molecular sciences · 2022
    Article
  3. Genome Profiling for Aflatoxin BG3 (Bethesda, Md.) · 2020
    Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Activation of aflatoxin B1 by expression of human CYP1A2 polymorphisms in Saccharomyces cerevisiae.Mutation research. Genetic toxicology and environmental mutagenesis · 2014
    Article
  9. Article
  10. Article
  11. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 2 institutions in 1 country.

Yingying GuoDepartmental of Environmental and Occupational Health Sciences, University of Washington, Seattle, Washington 98105-6099, USA.
Linda L Breeden
Helmut Zarbl
Bradley D Preston
David L Eaton
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Marian Esvelt · 1985 to 2026
$296.4M
XENOBIOTIC BIOTRANSFORMATION AND DISPOSITIONP30ES007033 · NIEHS · UNIVERSITY OF WASHINGTON · PI ALI SHOJAIE · 1995 to 2026
$42.5M
The FHCRC/UW Toxicogenomics ConsortiumU19ES011387 · NIEHS · UNIVERSITY OF WASHINGTON · PI ZARBL, HELMUT · 2001 to 2006
$7.7M
CELL CYCLE REGULATION OF THE YEAST HO GENER01GM041073 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BREEDEN, LINDA L. · 1994 to 2010
$5.4M
SPECIES DIFFERENCES IN GLUTATHIONE S-TRANSFERASESR01ES005780 · NIEHS · UNIVERSITY OF WASHINGTON · PI EATON, DAVID L · 1991 to 2003
$1.3M
NCI NIH HHS P30 CA015704NCI NIH HHS P30 CA15704NIEHS NIH HHS P30 ES007033NIEHS NIH HHS P30ES07033NIEHS NIH HHS R01 ES005780NIEHS NIH HHS R01ES05780NIEHS NIH HHS U19 ES011387NIEHS NIH HHS U19ES011387NIGMS NIH HHS R01 GM041073NIGMS NIH HHS R01GM41073
6 · The paper itself

Abstract

Aflatoxin B1 (AFB1) is a human hepatotoxin and hepatocarcinogen produced by the mold Aspergillus flavus. In humans, AFB1 is primarily bioactivated by cytochrome P450 1A2 (CYP1A2) and 3A4 to a genotoxic epoxide that forms N7-guanine DNA adducts. A series of yeast haploid mutants defective in DNA repair and cell cycle checkpoints were transformed with human CYP1A2 to investigate how these DNA adducts are repaired. Cell survival and mutagenesis following aflatoxin B1 treatment was assayed in strains defective in nucleotide excision repair (NER) (rad14), postreplication repair (PRR) (rad6, rad18, mms2, and rad5), homologous recombinational repair (HRR) (rad51 and rad54), base excision repair (BER) (apn1 apn2), nonhomologous end-joining (NHEJ) (yku70), mismatch repair (MMR) (pms1), translesion synthesis (TLS) (rev3), and checkpoints (mec1-1, mec1-1 rad53, rad9, and rad17). Together our data suggest the involvement of homologous recombination and nucleotide excision repair, postreplication repair, and checkpoints in the repair and/or tolerance of AFB1-induced DNA damage in the yeast model. Rev3 appears to mediate AFB1-induced mutagenesis when error-free pathways are compromised. The results further suggest unique roles for Rad5 and abasic endonuclease-dependent DNA intermediates in regulating AFB1-induced mutagenicity.

Indexed as

DNA DamageAflatoxin B1Base Pair MismatchCarcinogensCytochrome P-450 Enzyme SystemDNA RepairDNA ReplicationHumansMutationRecombination, GeneticSaccharomyces cerevisiaeAflatoxin B1CarcinogensCytochrome P-450 Enzyme System

Identifiers

PMID15988000
PMCPMC1168797
OpenAlexW2099438485

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.