Search results for "MAP kinase"

showing 10 items of 178 documents

Phosphorylation of extracellular signal-related protein kinase is required for rapid facilitation of heat-induced currents in rat dorsal root ganglio…

2005

A subgroup of dorsal root ganglion (DRG) neurons responds to noxious heat with an influx of cations carried by specific ion channels such as the transient receptor potential channel of the vanilloid receptor type, subtype 1 (TRPV1). Application of capsaicin induces a reversible facilitation of these currents. This facilitation could be an interaction of two agonists at their common receptor or be caused by an influx of calcium ions into the cell. Calcium influx into the cell can activate protein kinases such as the extracellular signal-related protein kinase (ERK) pathway. This study explored the kinetics, calcium-dependency and intracellular signals following application of capsaicin and l…

MaleMAPK/ERK pathwayHot TemperaturePatch-Clamp TechniquesStatistics as TopicTRPV1BiologyMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundBAPTAGanglia SpinalNitrilesButadienesAnimalsDrug InteractionsEnzyme InhibitorsPhosphorylationExtracellular Signal-Regulated MAP KinasesProtein kinase AProtein kinase CNeuronsAnalysis of VarianceDose-Response Relationship DrugGeneral NeuroscienceMEK inhibitorRatsCell biologychemistryBiochemistryCapsaicinMitogen-activated protein kinasebiology.proteinCalciumFemaleCapsaicinNeuroscience
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Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

MalePathologyTime Factorsp38 Mitogen-Activated Protein KinasesMiceVenulesLeukocytesEndothelial dysfunctionExtracellular Signal-Regulated MAP KinasesReceptorCells CulturedMice KnockoutMembrane GlycoproteinsAngiotensin IINF-kappa BArteriesEndothelial stem cellArteriolesNADPH Oxidase 5NADPH Oxidase 4NADPH Oxidase 2FemaleRNA InterferenceReceptors ChemokineTumor necrosis factor alphaCardiology and Cardiovascular MedicineSignal Transductionmedicine.medical_specialtyCX3C Chemokine Receptor 1BiologyTransfectionPeripheral blood mononuclear cellLosartanVeinsInterferon-gammaApolipoproteins EDownregulation and upregulationInternal medicineCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansLeukocyte RollingCX3CL1Chemokine CX3CL1Tumor Necrosis Factor-alphaEndothelial CellsMembrane ProteinsNADPH OxidasesAtherosclerosismedicine.diseaseAngiotensin IIMice Inbred C57BLDisease Models AnimalEndocrinologyAngiotensin II Type 1 Receptor BlockersArteriosclerosis, Thrombosis, and Vascular Biology
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2-Hydroxyoleate, a nontoxic membrane binding anticancer drug, induces glioma cell differentiation and autophagy

2012

Despite recent advances in the development of new cancer therapies, the treatment options for glioma remain limited, and the survival rate of patients has changed little over the past three decades. Here, we show that 2-hydroxyoleic acid (2OHOA) induces differentiation and autophagy of human glioma cells. Compared to the current reference drug for this condition, temozolomide (TMZ), 2OHOA combated glioma more efficiently and, unlike TMZ, tumor relapse was not observed following 2OHOA treatment. The novel mechanism of action of 2OHOA is associated with important changes in membrane-lipid composition, primarily a recovery of sphingomyelin (SM) levels, which is markedly low in glioma cells bef…

MaleProgrammed cell deathTime FactorsCell SurvivalMAP Kinase Signaling SystemCellular differentiationMice NudeAntineoplastic AgentsOleic AcidsBiologyglioma biomarkerfatty acidsMembrane LipidsMicePhosphatidylinositol 3-Kinases2-Hydroxyoleic AcidGliomaCell Line TumormedicineAutophagyTemozolomideAnimalsHumansPI3K/AKT/mTOR pathwayCell ProliferationMultidisciplinaryTemozolomideMicroscopy ConfocalDose-Response Relationship DrugCell growthCell MembraneRetinoblastoma proteinCell DifferentiationGliomaBiological Sciencesmedicine.diseaseXenograft Model Antitumor AssaysCell biologyDacarbazineProtein TransportCancer researchbiology.proteinras Proteinssphingomyelin synthaseProto-Oncogene Proteins c-aktcancer drug targetmedicine.drug
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Induction of RAGE Shedding by Activation of G Protein-Coupled Receptors

2011

The multiligand Receptor for Advanced Glycation End products (RAGE) is involved in various pathophysiological processes, including diabetic inflammatory conditions and Alzheimers disease. Full-length RAGE, a cell surface-located type I membrane protein, can proteolytically be converted by metalloproteinases ADAM10 and MMP9 into a soluble RAGE form. Moreover, administration of recombinant soluble RAGE suppresses activation of cell surface-located RAGE by trapping RAGE ligands. Therefore stimulation of RAGE shedding might have a therapeutic value regarding inflammatory diseases. We aimed to investigate whether RAGE shedding is inducible via ligand-induced activation of G protein-coupled recep…

MaleReceptors Vasopressinendocrine system diseasesReceptor for Advanced Glycation End Productslcsh:MedicineHydroxamic Acids570 Life sciencesRAGE (receptor)Adenylyl cyclaseADAM10 ProteinMicePhosphatidylinositol 3-Kinaseschemistry.chemical_compoundMolecular Cell BiologyNeurobiology of Disease and RegenerationSignaling in Cellular ProcessesMembrane Receptor SignalingReceptors Immunologiclcsh:ScienceReceptorLungCellular Stress ResponsesCalcium signalingMultidisciplinaryKinaseDipeptidesHormone Receptor SignalingCell biologyMatrix Metalloproteinase 9NeurologyReceptors OxytocinGene Knockdown Techniquescardiovascular systemMatrix Metalloproteinase 2Pituitary Adenylate Cyclase-Activating PolypeptideMedicineRNA InterferenceAdenylyl CyclasesResearch ArticleSignal Transduction570 Biowissenschaftenmedicine.medical_specialtyMAP Kinase Signaling SystemADAM17 ProteinBiologyAlzheimer DiseaseCa2+/calmodulin-dependent protein kinaseInternal medicinemedicineAnimalsHumansProtease InhibitorsCalcium Signalingcardiovascular diseasesBiologyG protein-coupled receptorlcsh:RHEK 293 cellsMembrane Proteinsnutritional and metabolic diseasesCyclic AMP-Dependent Protein KinasesADAM ProteinsG-Protein SignalingHEK293 CellsEndocrinologychemistryProteolysisDementialcsh:QAmyloid Precursor Protein SecretasesMolecular Neurosciencehuman activitiesReceptors Pituitary Adenylate Cyclase-Activating Polypeptide Type INeurosciencePLoS ONE
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Carboxyamidotriazole-Orotate Inhibits the Growth of Imatinib-Resistant Chronic Myeloid Leukaemia Cells and Modulates Exosomes-Stimulated Angiogenesis

2012

The Bcr/Abl kinase has been targeted for the treatment of chronic myelogenous leukaemia (CML) by imatinib mesylate. While imatinib has been extremely effective for chronic phase CML, blast crisis CML are often resistant. New therapeutic options are therefore needed for this fatal disease. Although more common in solid tumors, increased microvessel density was also reported in chronic myelogenous leukaemia and was associated with a significant increase of angiogenic factors, suggesting that vascularity in hematologic malignancies is a controlled process and may play a role in the leukaemogenic process thus representing an alternative therapeutic target. Carboxyamidotriazole-orotate (CTO) is …

MaleResearch ValidityPhysiologyAngiogenesisTumor PhysiologyFusion Proteins bcr-ablCancer Treatmentlcsh:MedicinePharmacologyExosomesCardiovascular PhysiologyBiochemistryPiperazinesHematologic Cancers and Related DisordersMicechemistry.chemical_compoundCell Movementhemic and lymphatic diseasesMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesPhosphorylationPost-Translational ModificationExtracellular Signal-Regulated MAP Kinaseslcsh:ScienceChronic Myelogenous LeukemiaMultidisciplinaryABLNeovascularization PathologicGene Expression Regulation LeukemicChemistryHematologyResearch AssessmentOncologyBenzamidesImatinib MesylateMedicineOncology AgentsAntiangiogenesis Therapymedicine.drugResearch ArticleChronic Myeloid LeukemiaAntineoplastic AgentsResearch and Analysis MethodsCell GrowthCell Line TumorLeukemia Myelogenous Chronic BCR-ABL PositiveLeukemiasCell AdhesionHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansRNA MessengerPhosphotyrosineBiologyCell ProliferationOrotic AcidTumor microenvironmentCarboxyamidotriazoleInterleukin-8lcsh:RBiology and Life SciencesProteinsCancers and NeoplasmsImatinibTriazolesmedicine.diseaseXenograft Model Antitumor AssaysRetractionExosomePyrimidinesImatinib mesylateDrug Resistance NeoplasmCarboxyamidotriazole Orotatelcsh:QAngiogenesisCell Adhesion MoleculesProto-Oncogene Proteins c-aktDevelopmental BiologyChronic myelogenous leukemiaPLoS ONE
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Retrograde neurotrophic signaling in rat retinal ganglion cells is transmitted via the ERK5 but not the ERK1/2 pathway.

2014

Purpose Neurotrophic deprivation is considered an important event in glaucomatous retinal ganglion cell (RGC) death. However, the mitogen-activated protein kinase (MAPK) pathway transmitting axonal neurotrophic signals in RGC has not been identified. We investigated the involvement of ERK5 and ERK1/2 in retrograde axonal neurotrophic signaling in rats. Methods Adult Sprague-Dawley rats were used. Retinal immunostaining for ERK5 and MEK5 was performed. Levels of total and phosphorylated ERK5 and ERK1/2 were analyzed in retinal lysate by quantitative Western blotting. The effects of age, brain-derived neurotrophic factor (BDNF) stimulation at RGC soma (intravitreal injection) or axon ending (…

MaleRetinal Ganglion Cellsmedicine.medical_specialtyAgingSuperior ColliculiMAP Kinase Signaling SystemBlotting WesternRetinal ganglionRetinaRats Sprague-Dawley03 medical and health sciences0302 clinical medicineNeurotrophic factorsInternal medicinemedicineAnimalsAxonPhosphorylationMitogen-Activated Protein Kinase 7030304 developmental biologyBrain-derived neurotrophic factorMitogen-Activated Protein Kinase 10303 health sciencesRetinaMitogen-Activated Protein Kinase 3biologyChemistryBrain-Derived Neurotrophic FactorBrainAnatomyRatsmedicine.anatomical_structureEndocrinologynervous systemRetinal ganglion cellTrk receptorOptic Nerve InjuriesIntravitreal Injectionsbiology.proteinsense organsNeuroglia030217 neurology & neurosurgeryNeurotrophinInvestigative ophthalmologyvisual science
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Morphological, molecular and hormonal adaptations to early morning versus afternoon resistance training

2018

It has been clearly established that maximal force and power is lower in the morning compared to noon or afternoon hours. This morning neuromuscular deficit can be diminished by regularly training in the morning hours. However, there is limited and contradictory information upon hypertrophic adaptations to time-of-day-specific resistance training. Moreover, no cellular or molecular mechanisms related to muscle hypertrophy adaptation have been studied with this respect. Therefore, the present study examined effects of the time-of-day-specific resistance training on muscle hypertrophy, phosphorylation of selected proteins, hormonal concentrations and neuromuscular performance. Twenty five pre…

MaleTime FactorsHydrocortisonePhysiologyMuscle ProteinsPhysiologylihaksetNoonp38 Mitogen-Activated Protein KinasesQuadriceps MuscleMuscle hypertrophy0302 clinical medicinePeptide Elongation Factor 2harjoitteluTestosteronePhosphorylationExtracellular Signal-Regulated MAP Kinasesta315vuorokausirytmiMorningRibosomal Protein S6resistanssiRibosomal Protein S6 Kinases 70-kDafood and beveragescell signallingAdaptation PhysiologicalMagnetic Resonance ImagingCircadian Rhythmmedicine.anatomical_structurevoimaharjoitteluhypertrophyAdultYoung Adult03 medical and health sciencesIsometric ContractionPhysiology (medical)medicineHumansMuscle Strengthdiurnalskeletal musclebusiness.industryfungiResistance trainingSkeletal muscle030229 sport sciencesresistance trainingbusinessBiomarkers030217 neurology & neurosurgeryHormoneChronobiology International
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Engineered microenvironments for synergistic VEGF - Integrin signalling during vascularization

2017

We have engineered polymer-based microenvironments that promote vasculogenesis both in vitro and in vivo through synergistic integrin-growth factor receptor signalling. Poly(ethyl acrylate) (PEA) triggers spontaneous organization of fibronectin (FN) into nanonetworks which provide availability of critical binding domains. Importantly, the growth factor binding (FNIII12-14) and integrin binding (FNIII9-10) regions are simultaneously available on FN fibrils assembled on PEA. This material platform promotes synergistic integrin/VEGF signalling which is highly effective for vascularization events in vitro with low concentrations of VEGF. VEGF specifically binds to FN fibrils on PEA compared to …

MaleVascular Endothelial Growth Factor AIntegrinsBiophysicsNeovascularization PhysiologicBioengineeringpoly(ethyl acrylate)ArticleBiomaterialsHuman Umbilical Vein Endothelial CellsImage Processing Computer-AssistedAnimalsHumansPhosphorylationExtracellular Signal-Regulated MAP KinasesFibronectinTissue EngineeringPhospholipase C gammaProtein assemblyVascularizationVEGFFibronectinsMice Inbred C57BLCellular MicroenvironmentMechanics of MaterialsFocal Adhesion Protein-Tyrosine KinasesFISICA APLICADAMutationCeramics and CompositesINGENIERIA ELECTRICAGrowth factorsProtein BindingSignal Transduction
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Receptor identification and physiological characterisation of glucagon-like peptide-2 in the rat heart.

2010

Abstract Background and aims The anorexigenic glucagon-like peptide (GLP)-2 is produced by intestinal L cells and released in response to food intake. It affects intestinal function involving G-protein-coupled receptors. To verify whether GLP-2 acts as a cardiac modulator in mammals, we analysed, in the rat heart, the expression of GLP-2 receptors and the myocardial and coronary responses to GLP-2. Methods and results GLP-2 receptors were detected on ventricular extracts by quantitative real-time polymerase chain reaction (Q-RT-PCR) and Western blotting. Cardiac GLP-2 effects were analysed on Langendorff perfused hearts. Intracellular GLP-2 signalling was investigated on Langendorff perfuse…

Maleendocrine systemmedicine.medical_specialtyCardiotonic AgentsNitric Oxide Synthase Type IIIMAP Kinase Signaling SystemG proteinEndocrinology Diabetes and MetabolismBlotting WesternMedicine (miscellaneous)Enzyme-Linked Immunosorbent AssayStimulationIn Vitro TechniquesBiologyReal-Time Polymerase Chain Reactionglucagon-like peptides-2 gut peptides cardiac performanceSettore BIO/09 - FisiologiaGlucagon-Like Peptide-1 Receptorchemistry.chemical_compoundInternal medicineCyclic AMPCyclic GMP-Dependent Protein KinasesGlucagon-Like Peptide 2Receptors GlucagonmedicineAnimalsCyclic adenosine monophosphatePhosphorylationRats WistarReceptorNutrition and Dieteticsdigestive oral and skin physiologyHeartPeptide FragmentsRatsPhospholambanEndocrinologyGene Expression RegulationchemistryInotropismGlucagon-Like Peptide-2 ReceptorCardiology and Cardiovascular MedicinecGMP-dependent protein kinasehormones hormone substitutes and hormone antagonistsIntestinal L CellsSignal Transduction
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Liver-specific p38α deficiency causes reduced cell growth and cytokinesis failure during chronic biliary cirrhosis in mice

2012

p38α mitogen-activated protein kinases (MAPK) may be essential in the up-regulation of proinflammatory cytokines and can be activated by transforming growth factor β, tumor necrosis factor-α, interleukin-1β, and oxidative stress. p38 MAPK activation results in hepatocyte growth arrest, whereas increased proliferation has been considered a hallmark of p38α-deficient cells. Our aim was to assess the role of p38α in the progression of biliary cirrhosis induced by chronic cholestasis as an experimental model of chronic inflammation associated with hepatocyte proliferation, apoptosis, oxidative stress, and fibrogenesis. Cholestasis was induced in wildtype and liver-specific p38α knockout mice by…

Malemedicine.medical_specialtyBiliary cirrhosisMAP Kinase Kinase 2ApoptosisBiologymedicine.disease_causeProinflammatory cytokineMitogen-Activated Protein Kinase 14MiceCholestasisInternal medicinemedicineAnimalsCyclin D1Cyclin B1Cell ProliferationCytokinesisMice KnockoutHepatologyLiver Cirrhosis BiliaryHepatologymedicine.diseaseMice Inbred C57BLSurvival RateDisease Models AnimalOxidative Stressmedicine.anatomical_structureEndocrinologyLiverHepatocyteChronic DiseaseDisease ProgressionHepatocytesTumor necrosis factor alphaOxidative stressSignal TransductionTransforming growth factorHepatology
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