ArticleFEBS letters2012
Ycf1p attenuates basal level oxidative stress response in Saccharomyces cerevisiae.
Article in FEBS letters, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
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Who cites it
5 citing papers in PubMed.
- The structural basis for regulation of the glutathione transporter Ycf1 by regulatory domain phosphorylation.Nature communications · 2022Article
- Overlapping responses between salt and oxidative stress in Debaryomyces hansenii.World journal of microbiology & biotechnology · 2019Article
- Sensitivity of Yeast Mutants Deficient in Mitochondrial or Vacuolar ABC Transporters to Pathogenesis-Related ProteinBiology · 2018Article
- Non-canonical regulation of glutathione and trehalose biosynthesis characterizes non-Microbial cell (Graz, Austria) · 2018Article
- Multiple glutathione disulfide removal pathways mediate cytosolic redox homeostasis.Nature chemical biology · 2013Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Ycf1p function is regulated by casein kinase 2α, Cka1p, via phosphorylation of Ser251. Cka1p-mediated phosphorylation of Ycf1p is attenuated in response to high salt stress. Previous results from our lab suggest a role for Ycf1p in cellular resistance to salt stress. Here, we show that Ycf1p plays an important role in cellular resistance to salt stress by maintaining the cellular redox balance via glutathione recycling. Our results suggest that during acute salt stress increased Sod1p, Sod2p and Ctt1p activity is the main compensatory for the loss in Ycf1p function that results from reduced Ycf1p-dependent recycling of cellular GSH levels.
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Registered trials
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