Search results for "Agoni"

showing 10 items of 2493 documents

p42 MAPK phosphorylates 80 kDa MARCKS at Ser-113.

1996

Abstract It is demonstrated here that p42 MAPKinase (p42 MAPK) phosphorylates the M yristoylated A lanine- R ich C - K inase S ubstrate (MARCKS) at Ser-113. In permeabilised Swiss 3T3 cells activation of protein kinase C (PKC) leads to p42 MAPK activation, but only the protein kinase C sites in MARCKS become phosphorylated and not Ser-113. The mitogen platelet-derived growth factor (PDGF) elicits the same response. These results demonstrate that while Ser-113 is a substrate for p42 MAPK in vitro and can be phosphorylated in vivo as shown by Taniguchi et al. [(1994) J. Biol. Chem. 269, 18299–18302], its phosphorylation is not subject to acute regulation by p42 MAPK in Swiss 3T3 cells.

MAPK/ERK pathwayMARCKSmedicine.medical_treatmentMitogen-activated protein kinase kinaseBiochemistryenvironment and public healthSubstrate SpecificityMiceStructural BiologySerinep42MAPKinasePhosphorylationMyristoylated Alanine-Rich C Kinase SubstrateCells CulturedProtein Kinase CMitogen-Activated Protein Kinase 1Platelet-Derived Growth FactorbiologyChemistryIntracellular Signaling Peptides and Proteins3T3 CellsProtein-Tyrosine KinasesCell biologyBiochemistryMitogen-activated protein kinasePhosphorylationTetradecanoylphorbol Acetatebiological phenomena cell phenomena and immunityPlatelet-derived growth factor receptorhormones hormone substitutes and hormone antagonistsendocrine systemRecombinant Fusion ProteinsMolecular Sequence DataBiophysicsGeneticsmedicineAnimalsAmino Acid SequenceMARCKSMolecular BiologyProtein kinase CGrowth factorMembrane ProteinsProteinsCell BiologyPeptide FragmentsEnzyme ActivationMolecular Weightenzymes and coenzymes (carbohydrates)Calcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMutagenesis Site-DirectedMitogensFEBS letters
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a1D-Adrenoceptors are responsible for the high sensitivity and the slow time-course of noradrenaline-mediated contraction in conductance arteries.

2013

The objective of this study was to determine whether the different time-course characteristics of α1-adrenoceptor-mediated contraction in arteries can be related to the subtypes involved. Contractile responses to noradrenaline (NA) were compared with inositol phosphate accumulation and extracellular signal-regulated kinase (ERK)1/2 phosphorylation after α1-agonist stimuli in the same vessels in the presence or absence of α1-antagonists in rat or in α1-subtype knockout (KO) mice. Aorta, where α1D-AR is the main functional subtype, had higher sensitivity to NA (in respect of inositol phosphate [IP], pERK1/2, and contractile response) than tail artery, where the α1A-adrenoceptor subtype is pre…

MAPK/ERK pathwaychemistry.chemical_classificationAgonistmedicine.medical_specialtyAortaContraction (grammar)business.industryKinasemedicine.drug_classcontraction time-courseconductance and resistance vesselsOriginal ArticlesEndocrinologyNeurologychemistryInternal medicinemedicine.arterymedicineExtracellularPhosphorylationGeneral Pharmacology Toxicology and Pharmaceuticsconductance and resistance vessels contraction time-course a1A-adrenoceptorsα1A-adrenoceptorsInositol phosphatebusiness
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Differential inhibition of TRAIL-mediated DR5-DISC formation by decoy receptors 1 and 2.

2006

International audience; Tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) is a member of the TNF family that induces cancer cell death by apoptosis with some selectivity. TRAIL-induced apoptosis is mediated by the transmembrane receptors death receptor 4 (DR4) (also known as TRAIL-R1) and DR5 (TRAIL-R2). TRAIL can also bind decoy receptor 1 (DcR1) (TRAIL-R3) and DcR2 (TRAIL-R4) that fail to induce apoptosis since they lack and have a truncated cytoplasmic death domain, respectively. In addition, DcR1 and DcR2 inhibit DR4- and DR5-mediated, TRAIL-induced apoptosis and we demonstrate here that this occurs through distinct mechanisms. While DcR1 prevents the assembly of the…

MESH : Hela CellsMESH: Membrane GlycoproteinsMESH: Membrane MicrodomainsDecoy Receptor 1ApoptosisMESH : Membrane GlycoproteinsReceptors Tumor Necrosis FactorTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing LigandJurkat Cells0302 clinical medicineMESH : Tumor Necrosis Factor Decoy ReceptorsMESH: Jurkat CellsDecoy receptorsReceptorCells CulturedMESH : Jurkat CellsMESH : Tumor Necrosis Factor-alpha0303 health sciencesMembrane GlycoproteinsMESH : Protein BindingArticlesMESH : Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsTumor Necrosis Factor Receptor-Associated Peptides and ProteinsCell biology030220 oncology & carcinogenesisCaspasesDeath-inducing signaling complexApoptosis/drug effects; Apoptosis Regulatory Proteins/antagonists & inhibitors; Apoptosis Regulatory Proteins/pharmacology; Caspases/metabolism; Cells Cultured; Death Domain Receptor Signaling Adaptor Proteins; Enzyme Activation/drug effects; GPI-Linked Proteins; HeLa Cells; Humans; Jurkat Cells; Membrane Glycoproteins/antagonists & inhibitors; Membrane Glycoproteins/pharmacology; Membrane Microdomains/drug effects; Protein Binding/drug effects; Receptors TNF-Related Apoptosis-Inducing Ligand; Receptors Tumor Necrosis Factor/metabolism; TNF-Related Apoptosis-Inducing Ligand; Tumor Necrosis Factor Decoy Receptors; Tumor Necrosis Factor Receptor-Associated Peptides and Proteins/metabolism; Tumor Necrosis Factor-alpha/antagonists & inhibitors; Tumor Necrosis Factor-alpha/pharmacologyMESH : Apoptosis Regulatory ProteinsMESH: TNF-Related Apoptosis-Inducing LigandProtein BindingMESH: Cells CulturedDeath Domain Receptor Signaling Adaptor ProteinsMESH: Enzyme ActivationBiologyMESH: Tumor Necrosis Factor Receptor-Associated Peptides and ProteinsGPI-Linked Proteins03 medical and health sciencesMembrane MicrodomainsCell surface receptorMESH : Cells Cultured[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyReceptors Tumor Necrosis Factor Member 10cHumansMESH: Protein Binding[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH: Receptors TNF-Related Apoptosis-Inducing LigandMESH : Receptors TNF-Related Apoptosis-Inducing LigandMolecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyDeath domainMESH: CaspasesMESH: HumansTumor Necrosis Factor-alphaMESH: Apoptosis Regulatory ProteinsMESH: ApoptosisMESH : HumansCell BiologyMESH: Receptors Tumor Necrosis FactorMESH: Tumor Necrosis Factor Decoy ReceptorsMESH : Receptors Tumor Necrosis FactorEnzyme ActivationMESH: Hela CellsReceptors TNF-Related Apoptosis-Inducing LigandTumor Necrosis Factor Decoy ReceptorsApoptosisMESH: Tumor Necrosis Factor-alphaMESH : Membrane MicrodomainsMESH : CaspasesApoptosis Regulatory ProteinsMESH : Enzyme ActivationMESH : ApoptosisMESH : Death Domain Receptor Signaling Adaptor ProteinsTumor Necrosis Factor Decoy ReceptorsHeLa CellsMESH: Death Domain Receptor Signaling Adaptor Proteins
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The human near-term myometrial beta 3-adrenoceptor but not the beta 2-adrenoceptor is resistant to desensitisation after sustained agonist stimulatio…

2004

International audience; 1. In order to compare the beta(2)- and beta(3)-adrenoceptor (beta-AR) desensitisation process in human near-term myometrium, we examined the influence of a pretreatment of myometrial strips with either a beta(2)- or a beta(3)-AR agonist (salbutamol or SR 59119A, respectively, both at 10 microm, for 5 and 15 h) on the relaxation and the cyclic adenosine monophosphate (cAMP) production induced by these agonists. 2. To assess some of the mechanisms potentially implicated in the beta-AR desensitisation process, we studied the influence of such treatment on the number of beta(2)- and beta(3)-AR binding sites, the beta(2)- and beta(3)-AR transcripts expression and the pho…

MESH : Receptors Adrenergic beta-3MESH : Adrenergic beta-AgonistsMESH : Receptors Adrenergic beta-2Adrenergic beta-3 Receptor AgonistsMESH : Analysis of VarianceMESH : Dose-Response Relationship DrugMESH: Adrenergic beta-Agonists[SDV.BC]Life Sciences [q-bio]/Cellular BiologyIn Vitro TechniquesMESH: Dose-Response Relationship DrugMESH: PregnancyPregnancyMESH: Analysis of VarianceHumansMESH: Protein BindingAlbuterolMESH : FemaleMESH : AlbuterolAdrenergic beta-2 Receptor Agonists[SDV.BC] Life Sciences [q-bio]/Cellular BiologyAnalysis of VarianceMESH: HumansDose-Response Relationship Drug[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyMESH : MyometriumMESH: AlbuterolMESH : HumansMESH : Protein BindingAdrenergic beta-AgonistsMESH : PregnancyReceptors Adrenergic beta-3PapersMyometriumMESH: MyometriumFemaleReceptors Adrenergic beta-2MESH: Receptors Adrenergic beta-3MESH: Receptors Adrenergic beta-2MESH: FemaleProtein Binding
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Choice of second-line disease-modifying antirheumatic drugs after failure of methotrexate therapy for rheumatoid arthritis: A decision tree for clini…

2009

Objective To survey rheumatologists' preferences for the choice of a second-line disease-modifying antirheumatic drug (DMARD) after inadequate response with methotrexate (MTX) therapy in rheumatoid arthritis (RA). Methods Thirty-six rheumatologists stated their preferences for RA treatment after inadequate response with MTX therapy (optimal dose at least 6 months). From the initial scenario, we derived 54 vignettes varying by rheumatoid factor or anti–cyclic citrullinated peptide antibody presence, swollen joint count, Disease Activity Score in 28 joints, and structural damage. Respondents stated their preference among 5 therapeutic options: MTX continuation, switch to another conventional …

MESH: Antirheumatic AgentsMESH: Decision TreesMESH: Treatment FailureArthritisMESH: Antibodies Anti-IdiotypicMESH: Logistic ModelsLogistic regressionSeverity of Illness IndexArthritis Rheumatoid0302 clinical medicineimmune system diseasesImmunology and AllergyMESH: Data CollectionPharmacology (medical)Treatment Failure030212 general & internal medicinePractice Patterns Physicians'skin and connective tissue diseasesMESH: Arthritis RheumatoidData CollectionAntibodies Anti-Idiotypic3. Good healthMESH: Interleukin 1 Receptor Antagonist ProteinMESH: Methotrexate[SDV.MHEP.RSOA]Life Sciences [q-bio]/Human health and pathology/Rhumatology and musculoskeletal systemAntirheumatic AgentsRheumatoid arthritismedicine.drugmusculoskeletal diseasesmedicine.medical_specialtyMESH: Rheumatoid FactorImmunologyPeptides Cyclic03 medical and health sciencesRheumatologyRheumatoid FactorMESH: Severity of Illness IndexInternal medicineSeverity of illnessmedicineHumansRheumatoid factorMESH: Physician's Practice PatternsMESH: Peptides Cyclic030203 arthritis & rheumatologyAnakinraMESH: HumansTumor Necrosis Factor-alphabusiness.industryDecision Treesmedicine.diseaseRheumatologyInterleukin 1 Receptor Antagonist ProteinLogistic ModelsMethotrexateMESH: Tumor Necrosis Factor-alphaPhysical therapyMethotrexatebusinessArthritis & Rheumatism
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TRAIL in cancer therapy: present and future challenges.

2007

International audience; Since its identification in 1995, TNF-related apoptosis-inducing ligand (TRAIL) has sparked growing interest in oncology due to its reported ability to selectively trigger cancer cell death. In contrast to other members of the TNF superfamily, TRAIL administration in vivo is safe. The relative absence of toxic side effects of this naturally occurring cytokine, in addition to its antitumoural properties, has led to its preclinical evaluation. However, despite intensive investigations, little is known in regards to the mechanisms underlying TRAIL selectivity or efficiency. An appropriate understanding of its physiological relevance, and of the mechanisms controlling ca…

MESH: Signal Transductionmedicine.medical_treatmentClinical BiochemistryApoptosisTRAILTNF-Related Apoptosis-Inducing LigandBioinformaticsTNF-Related Apoptosis-Inducing LigandMESH : TNF-Related Apoptosis-Inducing Ligand0302 clinical medicineDrug Delivery SystemsNeoplasmsDrug DiscoveryMESH: AnimalsMESH: Neoplasms0303 health sciencesTnf superfamily3. Good healthMESH : Antineoplastic AgentsCytokine030220 oncology & carcinogenesisMolecular MedicineMESH : Drug Delivery SystemsTRAIL-Receptors.Signal transductionMESH: TNF-Related Apoptosis-Inducing LigandSignal TransductionMESH: ForecastingProgrammed cell deathMESH: Drug Delivery SystemsCancer therapyAntineoplastic AgentsArticleresistance03 medical and health sciencesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyAnimalsHumanscancer[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : ForecastingTRAIL-receptor agonistic antibodies[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyPharmacologyMESH : Signal TransductionMESH: Humansbusiness.industryMESH: ApoptosisMESH : HumansCancermedicine.diseaseMESH : NeoplasmsCancer cellImmunologyMESH: Antineoplastic AgentsMESH : AnimalsbusinessTRAIL-ReceptorsMESH : ApoptosisForecasting
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MK801 blocks hypoxic blood-brain-barrier disruption and leukocyte adhesion.

2008

The aim of the present study was to examine the signaling pathways of hypoxia followed by reoxygenation (H/R)-induced disruption of the blood-brain-barrier (BBB) in a co-culture of astrocytes and brain endothelial cells (BEC) in vitro. We analyzed the possible stabilizing effect of MK801, a highly selective N-methyl-d-aspartate receptor (NMDAR) antagonist, on BBB integrity. Levels of reactive oxygen species (ROS), glutamate (Glut) release and monocyte adhesion were measured under normoxia and H/R. BBB integrity was monitored measuring the trans-endothelial electrical resistance (TEER). TEER values dropped under H/R conditions which was abolished by MK801. Glut release from astrocytes, but n…

Macrocyclic CompoundsSwineGlutamic AcidBiologyBlood–brain barrierchemistry.chemical_compoundmedicineExtracellularCell AdhesionElectric ImpedanceLeukocytesAnimalsEnzyme InhibitorsOxazolesCells Culturedchemistry.chemical_classificationReactive oxygen speciesRyanodine receptorRyanodineGeneral NeuroscienceEndoplasmic reticulumGlutamate receptorAcetophenonesBrainEndothelial CellsCell HypoxiaCoculture TechniquesCell biologyOxygenmedicine.anatomical_structurechemistryBlood-Brain BarrierAstrocytesApocyninCalciumNAD+ kinaseDizocilpine MaleateReactive Oxygen SpeciesExcitatory Amino Acid AntagonistsNeuroscience letters
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A newly established murine immature dendritic cell line can be differentiated into a mature state, but exerts tolerogenic function upon maturation in…

2007

AbstractThe phenotype and function of murine dendritic cells (DCs) are primarily studied using bone-marrow–derived DCs (BM-DCs), but may be hampered by the heterogenous phenotype of BM-DCs due to their differential state of maturation. Here we characterize a newly established murine DC line (SP37A3) of myeloid origin. During maintainance in the presence of granulocyte-macrophage colony-stimulating factor (GM-CSF) and M-CSF, SP37A3 cells resemble immature DCs characterized by low expression of major histocompatibility complex (MHC) II and costimulatory molecules and low T-cell stimulatory capacity. Upon stimulation, SP37A3 cells acquire a mature phenotype and activate naive T cells as potent…

Macrophage colony-stimulating factorMyeloidmedicine.medical_treatmentImmunologyBiologyMajor histocompatibility complexT-Lymphocytes RegulatoryBiochemistryDexamethasoneCell LineMicemedicineAnimalsGlucocorticoidsMyeloid Progenitor CellsCell ProliferationClonal AnergyMice Inbred BALB CFollicular dendritic cellsReceptors IgGHistocompatibility Antigens Class IICell DifferentiationDendritic CellsCell BiologyHematologyDendritic cellCoculture TechniquesUp-RegulationCell biologyInterleukin 1 Receptor Antagonist ProteinGranulocyte macrophage colony-stimulating factormedicine.anatomical_structureCytokineCell culturebiology.proteinCytokinesmedicine.drugBlood
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Synthesis and characterization of biotinylated and photoactivatable neuroleptics. Novel bifunctional probes for dopamine receptors

1992

Abstract We have synthesized and characterized a series of novel derivatives of established antagonists of the neurotransmitter dopamine, i.e. butyrophenones, hexahydrocarbolines and phenothiazenes. All derivatives were biotinylated, some of them carried an additional (photoactivatable) azido group. In the case of butyrophenones, the structural modifications were introduced at the aliphatic keto group and/or the heterocyclic ring system, both modifications resulting in significant decreases in binding affinity to dopamine D 2 and dopamine D 1 receptor subtypes. Biotinylation of hexahydrocarbolines significantly increased their binding affinity to D 1 receptors, with the affinity for D 2 rec…

Magnetic Resonance SpectroscopySpectrophotometry InfraredPhotochemistryButyrophenoneStereochemistryBiotinIn Vitro TechniquesLigandsBinding CompetitiveReceptors DopamineStructure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDopaminemedicineAnimalsNeurotransmitterReceptor030304 developmental biologyPharmacology0303 health sciencesDopamine antagonistAffinity LabelsBenzazepineschemistryBiochemistrySpiperoneDopamine receptorBiotinylationCattleButyrophenones030217 neurology & neurosurgeryAntipsychotic Agentsmedicine.drugEuropean Journal of Pharmacology: Molecular Pharmacology
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Temporally precise control of single-neuron spiking by juxtacellular nanostimulation

2017

Temporal patterns of action potentials influence a variety of activity-dependent intra- and intercellular processes and play an important role in theories of neural coding. Elucidating the mechanisms underlying these phenomena requires imposing spike trains with precisely defined patterns, but this has been challenging due to the limitations of existing stimulation techniques. Here we present a new nanostimulation method providing control over the action potential output of individual cortical neurons. Spikes are elicited through the juxtacellular application of short-duration fluctuating currents (“kurzpulses”), allowing for the sub-millisecond precise and reproducible induction of arbitr…

Male0301 basic medicine2-amino-5-phosphopentanoic acidPatch-Clamp TechniquesTime FactorsPhysiologyComputer scienceAction Potentialsgenetics [Luminescent Proteins]pharmacology [Valine]metabolism [Cytoskeletal Proteins]Mice0302 clinical medicineCortex (anatomy)physiology [Action Potentials]genetics [Nerve Tissue Proteins]6-Cyano-7-nitroquinoxaline-23-dioneNeuronsGeneral Neurosciencepharmacology [Excitatory Amino Acid Antagonists]Valinephysiology [Neurons]medicine.anatomical_structurepharmacology [6-Cyano-7-nitroquinoxaline-23-dione]FemaleSpike (software development)Neuroinformaticsgenetics [Synapsins]Models NeurologicalBiophysicsMice TransgenicNerve Tissue ProteinsOptogenetics03 medical and health sciencesmedicinedrug effects [Neurons]Animalsmetabolism [Synapsins]ddc:610metabolism [Luminescent Proteins]activity regulated cytoskeletal-associated proteingenetics [Cytoskeletal Proteins]analogs & derivatives [Valine]metabolism [Nerve Tissue Proteins]drug effects [Action Potentials]Somatosensory CortexSynapsinsElectric StimulationOptogeneticsCytoskeletal ProteinsLuminescent Proteins030104 developmental biologynervous systemInnovative Methodologycytology [Somatosensory Cortex]NeuronWhole cellExcitatory Amino Acid AntagonistsNeuroscience030217 neurology & neurosurgeryJournal of Neurophysiology
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