Search results for "MAP kinase"

showing 10 items of 178 documents

Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training

2014

This study investigated the effects of vitamin C and E supplementation on acute responses and adaptations to strength training. Thirty-two recreationally strength-trained men and women were randomly allocated to receive a vitamin C and E supplement (1000 mg day(-1) and 235 mg day(-1), respectively), or a placebo, for 10 weeks. During this period the participants' training involved heavy-load resistance exercise four times per week. Muscle biopsies from m. vastus lateralis were collected, and 1 repetition maximum (1RM) and maximal isometric voluntary contraction force, body composition (dual-energy X-ray absorptiometry), and muscle cross-sectional area (magnetic resonance imaging) were measu…

AdultMalemedicine.medical_specialtyJournal ClubPhysiologyStrength trainingMAP Kinase Signaling Systemmedicine.medical_treatmentMolecular and CellularMuscle ProteinsIsometric exerciseAscorbic AcidBiologyp38 Mitogen-Activated Protein KinasesMuscle hypertrophyIsometric ContractionInternal medicinemedicineHumansVitamin Eta315Leg pressMuscle SkeletalMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Vitamin Cta1184Vitamin EBiceps curlRibosomal Protein S6 Kinases 70-kDaResistance TrainingVitaminsAscorbic acidAdaptation PhysiologicalEndocrinologyDietary SupplementsFemale
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Enhancement of the FGFR1 signaling in the FGFR1-5-HT1A heteroreceptor complex in midbrain raphe 5-HT neuron systems. Relevance for neuroplasticity an…

2015

New findings show existence of FGFR1-5-HT1A heteroreceptor complexes in 5-HT nerve cells of the dorsal and median raphe nuclei of the rat midbrain and hippocampus. Synergistic receptor-receptor interactions in these receptor complexes indicated their enhancing role in hippocampal plasticity. The existence of FGFR1-5-HT1A heteroreceptor complexes also in midbrain raphe 5-HT nerve cells open up the possibility that antidepressant drugs by increasing extracellular 5-HT levels can cause an activation of the FGF-2/FGFR1 mechanism in these nerve cells as well. Therefore, the agonist modulation of the FGFR1-5-HT1A heteroreceptor complexes and their specific role is now determined in rat medullary …

AgonistSerotoninmedicine.medical_specialtymedicine.drug_classCellular differentiationBiophysicsHeteroreceptor complexBiologyHeteroreceptorBiochemistrySettore BIO/09 - FisiologiaCell LineMidbrainDorsal raphe nucleusMesencephalonInternal medicinemedicineAnimalsSerotonin 5-HT1A receptorReceptor Fibroblast Growth Factor Type 1Protein Interaction MapsPhosphorylationExtracellular Signal-Regulated MAP KinasesMolecular BiologyNeurons8-Hydroxy-2-(di-n-propylamino)tetralinNeuronal PlasticityRapheDepressionAnimalExtracellular Signal-Regulated MAP KinaseCell BiologySerotonin 5-HT1 Receptor AgonistsNeuronFibroblast growth factor receptorRatsEndocrinologymedicine.anatomical_structurenervous systemReceptor Serotonin 5-HT1AAutoreceptorRatFibroblast Growth Factor 2Serotonin 5-HT1 Receptor AgonistNeuronDimerizationNeuroscienceDepression; Dimerization; Fibroblast growth factor receptor; Heteroreceptor complex; Neuronal plasticity; Serotonin 5-HT1A receptor; 8-Hydroxy-2-(di-n-propylamino)tetralin; Animals; Cell Line; Extracellular Signal-Regulated MAP Kinases; Fibroblast Growth Factor 2; Mesencephalon; Neurons; Phosphorylation; Rats; Receptor Fibroblast Growth Factor Type 1; Receptor Serotonin 5-HT1A; Serotonin; Serotonin 5-HT1 Receptor Agonists; Neuronal Plasticity; Protein Interaction Maps
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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
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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)
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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
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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
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Biphasic Erk1/2 activation sequentially involving Gs and Gi signaling is required in beta3-adrenergic receptor-induced primary smooth muscle cell pro…

2013

Abstract The beta3 adrenergic receptor (B3-AR) reportedly induces cell proliferation, but the signaling pathways that were proposed, involving either Gs or Gi coupling, remain controversial. To further investigate the role of G protein coupling in B3-AR induced proliferation, we stimulated primary human myometrial smooth muscle cells with SAR150640 (B3-AR agonist) in the absence or presence of variable G-protein inhibitors. Specific B3-AR stimulation led to an Erk1/2 induced proliferation. We observed that the proliferative effects of B3-AR require two Erk1/2 activation peaks (the first after 3 min, the second at 8 h). Erk1/2 activation at 3 min was mimicked by forskolin (adenylyl-cyclase a…

Beta-3 adrenergic receptorGs alpha subunitMAP Kinase Signaling SystemMyocytes Smooth MuscleProliferationG protein coupled receptorBiologyGTP-Binding Protein alpha Subunits Gi-GoPertussis toxinchemistry.chemical_compoundErk1/2Protein kinasesCyclinsReceptors Adrenergic betaGTP-Binding Protein alpha Subunits GsHumansMolecular BiologyPI3K/AKT/mTOR pathwayCells CulturedG protein-coupled receptorCell ProliferationForskolinColforsinBeta-3 adrenergic receptorCell BiologyCell biologychemistryGene Expression RegulationPertussis ToxinMyometriumFemaleSignal transductionProto-oncogene tyrosine-protein kinase SrcBiochimica et Biophysica Acta (BBA) - Molecular Cell Research
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De novo design of protein kinase inhibitors by in silico identification of hinge region-binding fragments.

2013

Protein kinases constitute an attractive family of enzyme targets with high relevance to cell and disease biology. Small molecule inhibitors are powerful tools to dissect and elucidate the function of kinases in chemical biology research and to serve as potential starting points for drug discovery. However, the discovery and development of novel inhibitors remains challenging. Here, we describe a structure-based de novo design approach that generates novel, hinge-binding fragments that are synthetically feasible and can be elaborated to small molecule libraries. Starting from commercially available compounds, core fragments were extracted, filtered for pharmacophoric properties compatible w…

Binding SitesMolecular StructureProtein ConformationIntracellular Signaling Peptides and ProteinsArticlesProtein Serine-Threonine KinasesCrystallography X-RayMAP Kinase Kinase KinasesImmediate-Early ProteinsCSK Tyrosine-Protein KinaseMolecular Docking SimulationSmall Molecule Librariessrc-Family KinasesDrug DesignComputer SimulationProtein Kinase InhibitorsACS chemical biology
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ERK1 and ERK2 activation modulates diet-induced obesity in mice

2017

IF 3.112; International audience; Obesity is a worldwide problem, and dietary lipids play an important role in its pathogenesis. Recently, Erk1 knock-out (ERK1(-/-)) mice have been shown to exhibit low preference for dietary fatty acids. Hence, we maintained Erk1(-/-) mice on a high-fat diet (HFD) to assess the implication of this mitogen-activated protein (MAP) kinase in obesity. The Erk1(-/-) mice, fed the HFD, were more obese than wild-type (WT) animals, fed the same diet. Erk1(-/-) obese mice gained more fat and liver mass than WT obese animals. No difference was observed in daily food and energy intake in HFD-fed both group of animals. However, feed efficiency was higher in Erk1(-/-) t…

Blood GlucoseMale0301 basic medicinemedicine.medical_treatmentMice ObeseBiochemistryMicechemistry.chemical_compoundPhosphorylationBeta oxidationCells CulturedMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Reverse Transcriptase Polymerase Chain ReactionGeneral MedicineLipidsFatty acid synthaseLiverLipogenesisHomeostatic model assessmentmedicine.medical_specialtyBlotting WesternBiologyDiet High-FatReal-Time Polymerase Chain Reaction03 medical and health sciencesInsulin resistanceInternal medicinemedicineAnimals[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerObesity[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyInflammationTriglycerideLipogenesisInsulinBody WeightLipid Metabolismmedicine.diseaseObesityMice Inbred C57BL030104 developmental biologyEndocrinologychemistrybiology.proteinMAP kinaseInsulin ResistanceBiochimie
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Dual role of the p38 MAPK/cPLA2 pathway in the regulation of platelet apoptosis induced by ABT-737 and strong platelet agonists.

2013

p38 Mitogen-activated protein (MAP) kinase is involved in the apoptosis of nucleated cells. Although platelets are anucleated cells, apoptotic proteins have been shown to regulate platelet lifespan. However, the involvement of p38 MAP kinase in platelet apoptosis is not yet clearly defined. Therefore, we investigated the role of p38 MAP kinase in apoptosis induced by a mimetic of BH3-only proteins, ABT-737, and in apoptosis-like events induced by such strong platelet agonists as thrombin in combination with convulxin (Thr/Cvx), both of which result in p38 MAP kinase phosphorylation and activation. A p38 inhibitor (SB202190) inhibited the apoptotic events induced by ABT-737 but did not influ…

Blood PlateletsCancer ResearchcPLA2p38 mitogen-activated protein kinasesImmunologyBlotting Westernp38 Mitogen-Activated Protein KinasesPiperazinesNitrophenolsCellular and Molecular NeurosciencePhospholipase A2Crotalid VenomsHumansLectins C-Typeddc:610Cells CulturedMembrane Potential MitochondrialplateletSulfonamidesbiologyKinaseGroup IV Phospholipases A2Biphenyl CompoundsapoptosisConvulxinCell BiologyFlow Cytometryp38 MAP kinaseCell biologyApoptosisMitogen-activated protein kinasebiology.proteinPhosphorylationOriginal ArticleSignal transductionReactive Oxygen SpeciesSignal TransductionCell deathdisease
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