Search results for "eIF2α"

showing 2 items of 2 documents

Inappropriate translation inhibition and P-body formation cause cold-sensitivity in tryptophan-auxotroph yeast mutants

2017

In response to different adverse conditions, most eukaryotic organisms, including Saccharomyces cerevisiae, downregulate protein synthesis through the phosphorylation of eIF2α (eukaryotic initiation factor 2α) by Gcn2, a highly conserved protein kinase. Gcn2 also controls the translation of Gcn4, a transcription factor involved in the induction of amino acid biosynthesis enzymes. Here, we have studied the functional role of Gcn2 and Gcn2-regulating proteins, in controlling translation during temperature downshifts of TRP1 and trp1 yeast cells. Our results suggest that neither cold-instigated amino acid limitation nor Gcn2 are involved in the translation suppression at low temperature. Howev…

0301 basic medicineSaccharomyces cerevisiae ProteinsSaccharomyces cerevisiaeeIF2αSaccharomyces cerevisiaeProtein Serine-Threonine KinasesBiology03 medical and health sciencesPolysomeEukaryotic initiation factormedicineProtein biosynthesisLow temperatureEukaryotic Initiation FactorsPhosphorylationProtein kinase AMolecular BiologyTryptophanTranslation (biology)Cell Biologybiology.organism_classificationAdaptation PhysiologicalYeastHog1Cold TemperatureBasic-Leucine Zipper Transcription Factors030104 developmental biologyBiochemistryProtein BiosynthesisPolysomesSnf1Cold sensitivityPhosphorylationMitogen-Activated Protein Kinasesmedicine.symptomEnergy MetabolismGcn2 pathwayTranscription FactorsBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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eIF2α confers cellular tolerance to S. aureus α-toxin

2015

We report on the role of conserved stress-response pathways for cellular tolerance to a pore forming toxin. First, we observed that small molecular weight inhibitors including of eIF2α-phosphatase, jun-N-terminal kinase (JNK), and PI3-kinase sensitized normal mouse embryonal fibroblasts (MEFs) to the small pore forming S. aureus α-toxin. Sensitization depended on expression of mADAM10, the murine ortholog of a proposed high-affinity receptor for α-toxin in human cells. Similarly, eIF2α (S51A/S51A) MEFs, which harbor an Ala knock-in mutation at the regulated Ser51 phosphorylation site of eukaryotic translation initiation factor 2α, were hyper-sensitive to α-toxin. Inhibition of translation w…

lcsh:Immunologic diseases. AllergyMAPK/ERK pathwayImmunologyeIF2αBiologyCycloheximide03 medical and health scienceschemistry.chemical_compoundCellular toleranceImmunology and AllergyInitiation factorpore forming toxinsReceptorOriginal Research030304 developmental biologyGenetics0303 health sciencesKinase030302 biochemistry & molecular biologyJNK Mitogen-Activated Protein KinasesADAM10Translation (biology)MAPKCell biologyEIF2AK4chemistryPhosphorylationCytolysinS. aureus α-toxinlcsh:RC581-607Frontiers in Immunology
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