ArticleEMBO reports2011
Sir2 histone deacetylase prevents programmed cell death caused by sustained activation of the Hog1 stress-activated protein kinase.
Article in EMBO reports, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
What it found
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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.
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Who cites it
30 citing papers in PubMed, 52 citations in OpenAlex.
- Dynamic sumoylation is essential in yeast for suppressing stress-induced gene expression in non-stress conditions.Nucleic acids research · 2026Article
- Cytoplasmic sequestering of a fungal stress-activated MAPK in response to a host plant phenolic acid.PLoS pathogens · 2025Article
- The Viral K1 Killer Yeast System: Toxicity, Immunity, and Resistance.Yeast (Chichester, England) · 2024Review
- Advances inJournal of fungi (Basel, Switzerland) · 2023Review
- Article
- The roles of inducible chromatin and transcriptional memory in cellular defense system responses to redox-active pollutants.Free radical biology & medicine · 2021Review
- Developmental Roles of the Hog1 Protein Phosphatases of the Maize PathogenJournal of fungi (Basel, Switzerland) · 2021Article
- Article
- A genetic analysis reveals novel histone residues required for transcriptional reprogramming upon stress.Nucleic acids research · 2020Article
- Understanding MAPK Signaling Pathways in Apoptosis.International journal of molecular sciences · 2020Review
- Stress-Activated Protein Kinases in Human Fungal Pathogens.Frontiers in cellular and infection microbiology · 2019Review
- Oxidant-Sensing Pathways in the Responses of Fungal Pathogens to Chemical Stress Signals.Frontiers in microbiology · 2019Review
- THR1 mediates GCN4 and CDC4 to link morphogenesis with nutrient sensing and the stress response in Candida albicans.International journal of molecular medicine · 2018Article
- Article
- Overexpression of THI4 and HAP4 Improves Glucose Metabolism and Ethanol Production inFrontiers in microbiology · 2018Article
- Blocking two-component signalling enhances Candida albicans virulence and reveals adaptive mechanisms that counteract sustained SAPK activation.PLoS pathogens · 2017Article
- Stress-Activated Degradation of Sphingolipids Regulates Mitochondrial Function and Cell Death in Yeast.Oxidative medicine and cellular longevity · 2017Article
- Loss of Nat4 and its associated histone H4 N-terminal acetylation mediates calorie restriction-induced longevity.EMBO reports · 2016Article
- Role of Pex21p for Piggyback Import of Gpd1p and Pnc1p into Peroxisomes of Saccharomyces cerevisiae.The Journal of biological chemistry · 2015Article
- Osmostress-induced gene expression--a model to understand how stress-activated protein kinases (SAPKs) regulate transcription.The FEBS journal · 2015Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Exposure of yeast to high osmolarity induces a transient activation of the Hog1 stress-activated protein kinase (SAPK), which is required for cell survival under these conditions. However, sustained activation of the SAPK results in a severe growth defect. We found that prolonged SAPK activation leads to cell death, which is not observed in nma111 cells, by causing accumulation of reactive oxygen species (ROS). Mutations of the SCF(CDC4) ubiquitin ligase complex suppress cell death by preventing the degradation of Msn2 and Msn4 transcription factors. Accumulation of Msn2 and Msn4 leads to the induction of PNC1, which is an activator of the Sir2 histone acetylase. Sir2 is involved in protection against Hog1-induced cell death and can suppress Hog1-induced ROS accumulation. Therefore, cell death seems to be dictated by the balance of ROS induced by Hog1 and the protective effect of Sir2.
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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.