ArticlePloS one2013
Possible involvement of nitric oxide and reactive oxygen species in glucose deprivation-induced activation of transcription factor rst2.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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.
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Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- E2 ubiquitin-conjugating enzyme Ubc11 regulates Rst2 protein stability in the fission yeast Schizosaccharomyces pombe.Archives of microbiology · 2025Article
- A genome-wide analysis of carbon catabolite repression in Schizosaccharomyces pombe.BMC genomics · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Glucose is one of the most important sources of cellular nutrition and glucose deprivation induces various cellular responses. In Schizosaccharomyces pombe, zinc finger protein Rst2 is activated upon glucose deprivation, and regulates gene expression via the STREP (stress response element of Schizosaccharomyces pombe) motif. However, the activation mechanism of Rst2 is not fully understood. We monitored Rst2 transcriptional activity in living cells using a Renilla luciferase reporter system. Hydrogen peroxide (H2O2) enhanced Rst2 transcriptional activity upon glucose deprivation and free radical scavenger inhibited Rst2 transcriptional activity upon glucose deprivation. In addition, deletion of the trx2 (+) gene encoding mitochondrial thioredoxin enhanced Rst2 transcriptional activity. Notably, nitric oxide (NO) generators enhanced Rst2 transcriptional activity upon glucose deprivation as well as under glucose-rich conditions. Furthermore, NO specific scavenger inhibited Rst2 transcriptional activity upon glucose deprivation. Altogether, our data suggest that NO and reactive oxygen species may be involved in the activation of transcription factor Rst2.
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Registered trials
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