Search results for "PROTEIN KINASES"

showing 10 items of 427 documents

Influence of gene action across different time scales on behavior.

2002

Genes can affect natural behavioral variation in different ways. Allelic variation causes alternative behavioral phenotypes, whereas changes in gene expression can influence the initiation of behavior at different ages. We show that the age-related transition by honey bees from hive work to foraging is associated with an increase in the expression of the foraging ( for ) gene, which encodes a guanosine 3′,5′-monophosphate (cGMP)–dependent protein kinase (PKG). cGMP treatment elevated PKG activity and caused foraging behavior. Previous research showed that allelic differences in PKG expression result in two Drosophila foraging variants. The same gene can thus exert different types of influe…

AgingForagingGenes InsectHierarchy SocialBiologyGene expressionCyclic GMP-Dependent Protein KinasesAnimalsRNA MessengerAlleleSocial BehaviorGeneCyclic GMPAllelesIn Situ HybridizationMushroom BodiesGeneticsAppetitive BehaviorMultidisciplinaryBehavior AnimalDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingfungiBrainHoney beeFeeding BehaviorBeesPhenotypeUp-RegulationGene expression profilingPhenotypeMushroom bodiesDrosophilaScience (New York, N.Y.)
researchProduct

Tor-Sch9 deficiency activates catabolism of the ketone body-like acetic acid to promote trehalose accumulation and longevity

2014

In mammals, extended periods of fasting leads to the accumulation of blood ketone bodies including acetoacetate. Here we show that similar to the conversion of leucine to acetoacetate in fasting mammals, starvation conditions induced ketone body-like acetic acid generation from leucine in S. cerevisiae. Whereas wild-type and ras2Δ cells accumulated acetic acid, long-lived tor1Δ and sch9Δ mutants rapidly depleted it through a mitochondrial acetate CoA transferase-dependent mechanism, which was essential for lifespan extension. The sch9Δ-dependent utilization of acetic acid also required coenzyme Q biosynthetic genes and promoted the accumulation of intracellular trehalose. These results indi…

AgingSaccharomyces cerevisiae ProteinsKetoneLongevitySaccharomyces cerevisiaeSaccharomyces cerevisiaePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundAcetic acidSettore BIO/13 - Biologia ApplicataHumans2. Zero hungerchemistry.chemical_classificationbiologyCatabolismaging yeast nutrition acetic acid nutrientsTrehaloseOriginal ArticlesCell Biologybiology.organism_classificationchronological lifespanTrehaloseacetic acidSch9chemistryBiochemistryCoenzyme Q – cytochrome c reductaseKetone bodiesleucineLeucineProtein KinasesAging Cell
researchProduct

Protein kinase activities associated with ribosomes of developing rat brain. Identification of eukaryotic initiation factor 2 kinases.

1986

Protein kinases associated with ribosomes in the brains of suckling (4-10 days) and adult (2 months) rats were extracted from ribosomal fraction with 0.5 M KCl. The different protein kinase activities were characterized by their ability to phosphorylate three exogenous substrates: casein, histone IIs and histone IIIs in the presence of different modulators. Ribosomal salt wash fractions contain a high casein kinase activity which was partially inhibited by heparin and stimulated by calmodulin in the presence of Ca2+, indicating the presence of casein kinase I and II and calcium/calmodulin-dependent kinases. Cyclic AMP and cyclic GMP-dependent kinases and protein kinase C (calcium/phospholip…

AgingbiologyCyclin-dependent kinase 2BrainCaseinsRats Inbred StrainsMitogen-activated protein kinase kinaseRatseIF-2 KinaseDevelopmental NeuroscienceBiochemistryCasein Kinase ICasein kinase 2 alpha 1biology.proteinAnimalsASK1Cyclin-dependent kinase 9Casein kinase 1Casein kinase 2PhosphorylationProtein KinasesRibosomesDevelopmental BiologySubcellular FractionsInternational journal of developmental neuroscience : the official journal of the International Society for Developmental Neuroscience
researchProduct

Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
researchProduct

Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression.

1999

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mito…

Alkylating AgentsProto-Oncogene Proteins c-junUltraviolet RaysStimulationBiologyenvironment and public healthWortmanninTransactivationchemistry.chemical_compoundMiceAnimalsPhosphatidylinositolCollagenasesProtein kinase AMolecular BiologyCell Growth and DevelopmentMitogen-Activated Protein Kinase 1Kinasec-junJNK Mitogen-Activated Protein KinasesCell Biology3T3 CellsMethyl MethanesulfonateMolecular biologyAndrostadienesEnzyme ActivationGene Expression Regulation NeoplasticTranscription Factor AP-1chemistryCalcium-Calmodulin-Dependent Protein KinasesPhosphorylationMitogen-Activated Protein KinasesWortmanninMolecular and cellular biology
researchProduct

Detection of mitochondrial electron chain carrier redox status by transhepatic light intensity during rat liver reperfusion.

2003

The aim of the study was to investigate mitochondrial electron transfer during rat liver reperfusion after cold storage and hypothermic machine perfusion. Livers from male Brown Norway rats were preserved (UW) for 10h either by cold storage (CS) or by hypothermic oxygenated perfusion extracorporal (HOPE). Transhepatic photometric analysis allowed determination of the redox status of mitochondrial cytochromes during preservation, rewarming and reperfusion. Mitochondrial electron chain carriers were inhibited at different sites with rotenone and cyanide in some experiments. reversed transcriptional polymerase chain reaction (RT-PCR) was performed after reperfusion concerning transcription of …

AnionsMaleTime FactorsCytochromeLightCold storageCaspase 3ElectronsDNA FragmentationMitochondrionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundSuperoxidesAnimalsCaspase-9CryopreservationCyanidesbiologySuperoxideCaspase 3Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesTemperatureNADH DehydrogenaseGeneral MedicineRotenoneDNAOrgan PreservationLipid MetabolismCaspase 9MitochondriaRatsCold TemperatureOxygenLight intensitychemistryBiochemistryElectron Transport Chain Complex ProteinsLiverCaspasesReperfusionbiology.proteinCytochromesLipid PeroxidationMitogen-Activated Protein KinasesGeneral Agricultural and Biological SciencesReactive Oxygen SpeciesOxidation-ReductionCryobiology
researchProduct

A role for the MAP kinase gene MKC1 in cell wall construction and morphological transitions in Candida albicans.

1998

The Candida albicans MKC1 gene encodes a mitogen-activated protein (MAP) kinase, which has been cloned by complementation of the lytic phenotype associated with Saccharomyces cerevisiae slt2 (mpk1) mutants. In this work, the physiological role of this MAP kinase in the pathogenic fungus C. albicans was characterized and a role for MKC1 in the biogenesis of the cell wall suggested based on the following criteria. First, C. albicans mkc1Δ/mkc1Δ strains displayed alterations in their cell surfaces under specific conditions as evidenced by scanning electron microscopy. Second, an increase in specific cell wall epitopes (O-glycosylated mannoprotein) was shown by confocal microscopy in mkc1Δ/mkc1…

Antifungal AgentsTranscription GeneticSaccharomyces cerevisiaeMutantMAP Kinase Kinase 2MAP Kinase Kinase 1ChitinSaccharomyces cerevisiaeProtein Serine-Threonine KinasesMicrobiologyGene Expression Regulation EnzymologicFungal ProteinsPseudohyphal growthCell WallGene Expression Regulation FungalCandida albicansCandida albicansDNA FungalFluorescent Antibody Technique IndirectGlucansProtein Kinase CMitogen-Activated Protein Kinase KinasesRecombination GeneticMembrane GlycoproteinsMicroscopy ConfocalbiologyKinaseProtein-Tyrosine Kinasesbiology.organism_classificationFlow Cytometrybeta-GalactosidaseCorpus albicansComplementationMicroscopy ElectronBiochemistryMitogen-activated protein kinaseCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMicroscopy Electron ScanningMitogen-Activated Protein KinasesPlasmidsMicrobiology (Reading, England)
researchProduct

Thiol antioxidants block the activation of antigen-presenting cells by contact sensitizers.

2003

Strong contact sensitizers are able to induce signal transduction mechanisms such as tyrosine phosphorylation and activation of MAP kinases in antigen-presenting cells. We studied the capacity of different antioxidants (ascorbic acid, alpha-tocopherol, pyrrolidine dithiocarbamate, N-acetylcysteine, and glutathione) to block the increase in tyrosine phosphorylation in human monocytes seen after stimulation with strong contact sensitizers. Human peripheral blood mononuclear cells were stimulated with 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone in the presence or absence of these antioxidants. The total amount of membrane-associated phosphotyrosine in CD14+ cells was quantifi…

Antigen-Presenting CellsDermatologyPicryl ChlorideDermatitis ContactBiochemistryAntioxidantschemistry.chemical_compoundPyrrolidine dithiocarbamateHumansdendritic cellsCysteineSulfhydryl CompoundsTyrosinePhosphorylationAntigen-presenting cellMolecular BiologyCells CulturedNF-kappa BTyrosine phosphorylationCell BiologyGlutathioneAscorbic acidGlutathioneAcetylcysteineMAP kinaseschemistryBiochemistrycontact sensitizerthiol antioxidantTyrosineSignal transductionMitogen-Activated Protein KinasesmonocytesCysteineThe Journal of investigative dermatology
researchProduct

Mycobacterial antigen(s) induce anergy by altering TCR- and TCR/CD28-induced signalling events: insights into T-cell unresponsiveness in leprosy.

2009

Present study investigates the role of Mycobacterium leprae (M. leprae) antigens on TCR- and TCR/CD28-induced signalling leading to T-cell activation and further correlates these early biochemical events with T-cell anergy, as prevailed in advanced stages of leprosy. We observed that both whole cell lystae (WCL) and soluble fraction of M. leprae sonicate (MLSA) not only inhibited TCR, thapsigargin and ionomycin induced calcium fluxes by diminishing the opening of calcium channels, but also TCR- or TCR/CD28-induced proximal signalling events like phosphorylation of Zap-70 and protein kinase-C (PKC) activity. Study of TCR- and TCR/CD28-induced downstream signals revealed that M. leprae antige…

Antigens Differentiation T-LymphocyteMAP Kinase Signaling SystemT cellT-LymphocytesImmunologyReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyLymphocyte ActivationJurkat cellsp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundJurkat CellsCD28 AntigensAntigens CDLeprosyCalcium fluxmedicineHumansLectins C-TypeEnzyme InhibitorsPromoter Regions GeneticMolecular BiologyMycobacterium lepraeProtein Kinase CCell ProliferationClonal AnergyAntigens BacterialMitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinaseIonophoresNFATC Transcription FactorsIonomycinT-cell receptorInterleukin-2 Receptor alpha SubunitCD28hemic and immune systemsNFATbiology.organism_classificationCell biologyMycobacterium lepraemedicine.anatomical_structurechemistryGene Expression RegulationIonomycinImmunologyInterleukin-2ThapsigarginCalciumMolecular immunology
researchProduct

The Fumarate/Succinate Antiporter DcuB of Escherichia coli Is a Bifunctional Protein with Sites for Regulation of DcuS-dependent Gene Expression

2008

DcuB of Escherichia coli catalyzes C4-dicarboxylate/succinate antiport during growth by fumarate respiration. The expression of genes of fumarate respiration, including the genes for DcuB (dcuB) and fumarate reductase (frdABCD) is transcriptionally activated by C4-dicarboxylates via the DcuS-DcuR two-component system, comprising the sensor kinase DcuS, which contains a periplasmic sensing domain for C4-dicarboxylates. Deletion or inactivation of dcuB caused constitutive expression of DcuS-regulated genes in the absence of C4-dicarboxylates. The effect was specific for DcuB and not observed after inactivation of the homologous DcuA or the more distantly related DcuC transporter. Random and s…

AntiporterMutantlac operonBiologymedicine.disease_causePeptide MappingBiochemistryAntiportersFumaratesEscherichia colimedicineMolecular BiologyEscherichia coliDerepressionDicarboxylic Acid TransportersIon TransportEscherichia coli ProteinsMutagenesisSuccinatesGene Expression Regulation BacterialCell BiologyPeriplasmic spaceFumarate reductaseDNA-Binding ProteinsSuccinate DehydrogenaseAmino Acid SubstitutionBiochemistryGene Knockdown TechniquesMutagenesis Site-DirectedProtein KinasesTranscription FactorsJournal of Biological Chemistry
researchProduct