Evidence map›Paper›PMID 17919749›Full record

ArticleBiochimica et biophysica acta2008

Disruption of aldo-keto reductase genes leads to elevated markers of oxidative stress and inositol auxotrophy in Saccharomyces cerevisiae.

Qing Chang, J Mark Petrash

Abstract read
In one paragraph

Article in Biochimica et biophysica acta, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

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  10. Overexpression of aldo-keto-reductase in azole-resistant clinical isolates of Candida glabrata determined by cDNA-AFLP.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2013
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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

2 authors at 1 institution in 1 country.

Qing ChangDepartment of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, MO 63110-3018, USA.
J Mark Petrash
Washington University in St. Louis · US

Funding

WASHINGTON UNIVERSITY CENTER VISION RESEARCHP30EY002687 · NEI · WASHINGTON UNIVERSITY · PI Philip Andrew Ruzycki · 1985 to 2026
$18.4M
MOLECULAR BIOLOGY OF ALDOSE REDUCTASE AND CATARACTR01EY005856 · NEI · WASHINGTON UNIVERSITY · PI PETRASH, JONATHAN MARK · 1988 to 2014
$6.8M
MOLECULAR STUDIES OF ALDOSE REDUCTASE AND CATARACTR23EY005856 · NEI · EMORY UNIVERSITY · PI PETRASH, JONATHAN MARK · 1985 to 1987
–
MOLECULAR BIOLOGY OF ALDOSE REDUCTASE AND CATARACTR55EY005856 · NEI · WASHINGTON UNIVERSITY · PI PETRASH, JONATHAN MARK · 1991 to 1991
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NEI NIH HHS EY02687NEI NIH HHS EY05856NEI NIH HHS P30 EY002687NEI NIH HHS R01 EY005856
6 · The paper itself

Abstract

A large family of aldo-keto reductases with similar kinetic and structural properties but unknown physiological roles is expressed in the yeast Saccharomyces cerevisiae. Strains with one or two AKR genes disrupted have apparently normal phenotypes, but disruption of at least three AKR genes results in a heat shock phenotype and slow growth in inositol-deficient culture medium (Ino(-)). The present study was carried out to identify metabolic or signaling defects that may underlie phenotypes that emerge in AKR deficient strains. Here we demonstrate that pretreatment of a pentuple AKR null mutant with the anti-oxidative agent N-acetyl-cysteine rescues the heat shock phenotype. This indicates that AKR gene disruption may be associated with defects in oxidative stress response. We observed additional markers of oxidative stress in AKR-deficient strains, including reduced glutathione levels, constitutive nuclear localization of the oxidation-sensitive transcription factor Yap1 and upregulation of a set of Yap1 target genes whose function as a group is primarily involved in response to oxidative stress and redox balance. Genetic analysis of the Ino(-) phenotype of the null mutants showed that defects in transcriptional regulation of the INO1, which encodes for inositol-1-phosphate synthase, can be rescued through ectopic expression of a functional INO1. Taken together, these results suggest potential roles for AKRs in oxidative defense and transcriptional regulation.

Indexed as

Autotrophic ProcessesGene DeletionOxidative StressAlcohol OxidoreductasesAldehyde ReductaseAldo-Keto ReductasesBiomarkersCell NucleusCyclic AMP-Dependent Protein KinasesGene Expression Regulation, FungalGenes, FungalGlycogenInositolPhenotypeProtein Transportras ProteinsAlcohol OxidoreductasesAldehyde ReductaseAldo-Keto ReductasesBiomarkersCyclic AMP-Dependent Protein KinasesGlycogenInositolras ProteinsSaccharomyces cerevisiae ProteinsTranscription FactorsYAP1 protein, S cerevisiae

Identifiers

PMID17919749
PMCPMC2254213
OpenAlexW2102657099

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.