Search results for "Growth Inhibitors"

showing 4 items of 24 documents

Exclusion of Saccharomyces kudriavzevii from a wine model system mediated by Saccharomyces cerevisiae.

2010

This study investigated the competition and potential hybrid generation between the species Saccharomyces cerevisiae and S. kudriavzevii in a wine-model environment. Our main goal was to understand why S. kudriavzevii has not been found in wine fermentations whilst their hybrids are present. Auxotrophic mutants (Ura(-) and Lys(-)) were used to favour the selection of hybrids and to specifically differentiate the two species in mixed fermentations carried out at different temperatures (17 °C, 24 °C and 31 °C). Both yeasts showed a reduction in their maximum specific growth rates in mixed fermentations, indicating a clear antagonistic effect between the two microorganisms. Temperature played …

media_common.quotation_subjectPopulationSaccharomyces cerevisiaeBioengineeringWineApplied Microbiology and BiotechnologyBiochemistrySaccharomycesCompetition (biology)SaccharomycesBotanyAntibiosisGeneticsFood scienceSelection Geneticeducationmedia_commonWineFermentation in winemakingRecombination Geneticeducation.field_of_studybiologyEthanolTemperaturefood and beveragesbiology.organism_classificationGrowth InhibitorsFermentationFermentationSaccharomyces kudriavzeviiBiotechnologyYeast (Chichester, England)
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Ethanol inhibits astroglial cell proliferation by disruption of phospholipase D-mediated signaling.

2002

The activation of phospholipase D (PLD) is a common response to mitogenic stimuli in various cell types. As PLD-mediated signaling is known to be disrupted in the presence of ethanol, we tested whether PLD is involved in the ethanol-induced inhibition of cell proliferation in rat cortical primary astrocytes. Readdition of fetal calf serum (FCS) to serum-deprived astroglial cultures caused a rapid, threefold increase of PLD activity and a strong mitogenic response; both effects were dependent on tyrosine kinases but not on protein kinase C. Ethanol (0.1-2%) suppressed the FCS-induced, PLD-mediated formation of phosphatidic acid (PA) as well as astroglial cell proliferation in a concentration…

medicine.medical_specialtyPlatelet-derived growth factorIndolestert-Butyl Alcoholmedicine.medical_treatmentButanolsBecaplerminPhosphatidic AcidsNerve Tissue ProteinsBiologyBiochemistryCulture Media Serum-FreeCellular and Molecular Neurosciencechemistry.chemical_compound1-ButanolInternal medicineLysophosphatidic acidmedicinePhospholipase DAnimalsPhosphorylationProtein kinase APlatelet-Derived Growth FactorEndothelin-1EthanolPhospholipase DCell growthGrowth factorPhosphatidic acidDNAProto-Oncogene Proteins c-sisProtein-Tyrosine KinasesGenisteinGrowth InhibitorsCell biologyRatsEndocrinologychemistryFetal Alcohol Spectrum DisordersAstrocyteslipids (amino acids peptides and proteins)Signal transductionVanadatesProtein Processing Post-TranslationalCell DivisionSignal TransductionJournal of neurochemistry
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Oncostatin M, leukaemia-inhibitory factor and interleukin 6 trigger different effects on alpha1-proteinase inhibitor synthesis in human lung-derived …

1998

Interleukin 6 (IL-6), oncostatin M (OSM) and leukaemia-inhibitory factor (LIF) share a common signal-transducing subunit in each of their receptors and thus mediate an overlapping spectrum of biological activities. Although all of these cytokines stimulate the production of α1-proteinase inhibitor (α1-PI) in hepatocyte-derived cells, only OSM is able to up-regulate levels of this inhibitor in epithelial cells originating from the lung. In this study we characterized human lung-derived epithelial-like HTB58 cells for their ability to synthesize α1-PI after treatment with IL-6, OSM and LIF. The results demonstrate that the resistance of HTB58 cells to the effects of IL-6 and LIF was not becau…

medicine.medical_specialtyendocrine systemProtein subunitBlotting WesternOncostatin MInhibitory postsynaptic potentialBiochemistryLeukemia Inhibitory FactorInternal medicinemedicineTumor Cells CulturedHumansInterleukin 6ReceptorMolecular BiologyLungLymphokinesbiologyChemistryInterleukin-6fungiOncostatin MOncostatin M receptorEpithelial CellsCell BiologyGlycoprotein 130Blotting NorthernGrowth InhibitorsCell biologyInterleukin 31Endocrinologyalpha 1-Antitrypsinbiology.proteinPeptidesResearch ArticleThe Biochemical journal
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INHIBITION OF CELLULAR GROWTH AND STEROID 11β-HYDROXYLATION INRAS-TRANSFORMED ADRENOCORTICAL CELLS BY THE FUNGAL TOXINS BETICOLINS

1996

Abstract The proliferation of GM16 and 4CDTras-transformed newborn rat adrenocortical (RTAC) cells and Y1 mouse adrenal tumor cells was inhibited by beticolins, the fungal toxins extracted fromCercospora beticola, at submicromolar concentrations in a dose-dependent manner. Inhibitory concentrations for half the maximum inhibition were 150, 75 and 25 n M for beticolin-1 and 230, 150 and 50 n M for beticolin-2 in GM16, 4CDT and Y1 cells respectively. Beticolins strongly inhibited the production of 11β-hydroxysteroids on the second and third days of treatment in a dose-dependent manner between 0.1 and 1 μ M . Beticolins were shown by confocal microscopy to be localized in cytoplasmic organelle…

medicine.medical_treatmentAdrenal Gland NeoplasmsBiologyTransfectionHeterocyclic Compounds 4 or More RingsSteroidlaw.inventionHydroxylationMiceStructure-Activity Relationshipchemistry.chemical_compoundConfocal microscopylawOrganelleTumor Cells CulturedmedicineAnimalsCells CulturedHydroxysteroidsMicroscopy ConfocalDose-Response Relationship DrugCell growthCell BiologyGeneral MedicineMycotoxinsGrowth InhibitorsNeoplasm ProteinsRatsCell Transformation NeoplasticGenes rasAnimals NewbornchemistryBiochemistryCytoplasmAdrenal CortexSteroid 11-beta-HydroxylaseSignal transductionGrowth inhibitionCell DivisionCell Biology International
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