Search results for "Azine"

showing 10 items of 1589 documents

Cannabinoid receptor 1 modulates the autophagic flux independent of mTOR- and BECLIN1-complex

2013

Cannabinoid Receptor 1 (CB1) has been initially described as the receptor for Delta-9-Tetrahydrocannabinol in the central nervous system (CNS), mediating retrograde synaptic signaling of the endocannabinoid system. Beside its expression in various CNS regions, CB1 is ubiquituous in peripheral tissues, where it mediates, among other activities, the cell's energy homeostasis. We sought to examine the role of CB1 in the context of the evolutionarily conserved autophagic machinery, a main constituent of the regulation of the intracellular energy status. Manipulating CB1 by siRNA knockdown in mammalian cells caused an elevated autophagic flux, while the expression of autophagy-related genes rema…

Cannabinoid receptorMorpholinesGreen Fluorescent ProteinsDown-RegulationmTORC1NaphthalenesBiochemistryMiceCellular and Molecular NeurosciencePiperidinesReceptor Cannabinoid CB1RimonabantAutophagymedicineAnimalsHumansEnzyme InhibitorsCannabinoid Receptor AntagonistsCells CulturedPI3K/AKT/mTOR pathwayAdenine NucleotidesChemistryTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCalcium Channel BlockersEmbryo MammalianEndocannabinoid systemBenzoxazinesCell biologyMice Inbred C57BLnervous systemAstrocytesPyrazolesBeclin-1lipids (amino acids peptides and proteins)MacrolidesSynaptic signalingRimonabantApoptosis Regulatory ProteinsFlux (metabolism)medicine.drugJournal of Neurochemistry
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WIN 55,212-2, agonist of cannabinoid receptors, prevents amyloid β1-42 effects on astrocytes in primary culture

2015

Alzheimer's disease (AD), a neurodegenerative illness involving synaptic dysfunction with extracellular accumulation of Aβ1-42 toxic peptide, glial activation, inflammatory response and oxidative stress, can lead to neuronal death. Endogenous cannabinoid system is implicated in physiological and physiopathological events in central nervous system (CNS), and changes in this system are related to many human diseases, including AD. However, studies on the effects of cannabinoids on astrocytes functions are scarce. In primary cultured astrocytes we studied cellular viability using MTT assay. Inflammatory and oxidative stress mediators were determined by ELISA and Western-blot techniques both in…

Cannabinoid receptormedicine.medical_treatmentInterleukin-1betaNitric Oxide Synthase Type IIlcsh:Medicinemedicine.disease_causeReceptors CannabinoidWIN 55212-2Receptorlcsh:ScienceCerebral CortexMultidisciplinaryCalcium Channel BlockersSistema nerviós Malaltiesmedicine.symptomSignal transductionResearch ArticleSignal Transductionmedicine.drugmedicine.medical_specialtyCell SurvivalMorpholinesPrimary Cell CultureInflammationNaphthalenesBiologyNeurologiaFetusInternal medicinemedicineAnimalsViability assayCannabinoid Receptor AgonistsAmyloid beta-PeptidesSuperoxide DismutaseTumor Necrosis Factor-alphalcsh:RTranscription Factor RelAPeptide FragmentsBenzoxazinesRatsPPAR gammaOxidative StressEndocrinologyGene Expression RegulationCyclooxygenase 2Astrocyteslcsh:QFisiologia humanaCannabinoidOxidative stress
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Carbachol-induced network oscillations in the intact cerebral cortex of the newborn rat.

2003

In mature cortex, activation of the cholinergic system induces oscillatory network activity and facilitates synaptic plasticity. We used an in vitro preparation of the intact cerebral cortex and cortical slices of the neonatal rat to study carbachol (CCh, >or=30 micro M)-induced network oscillations during the early postnatal period. Multi-site extracellular recordings revealed CCh-induced transient beta oscillations with an average duration of 4.6 +/- 0.2 s, amplitude of 123 +/- 7.4 microV and frequency of 17.7 +/- 0.5 Hz. These oscillations propagated uniformly at 0.5-1.5 mm/s over the cortex and were reversibly blocked by tetrodotoxin (TTX) and atropine, indicating that they depended on …

CarbacholCognitive NeuroscienceKainate receptorAMPA receptorIn Vitro TechniquesCellular and Molecular Neurosciencechemistry.chemical_compoundBiological ClocksCortex (anatomy)medicineAnimalsRats WistarCerebral CortexRatsmedicine.anatomical_structurechemistryAnimals NewbornCholinergic FibersCerebral cortexCNQXBiophysicsGabazineNMDA receptorCarbacholNerve NetNeurosciencemedicine.drugCerebral cortex (New York, N.Y. : 1991)
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The Synthetic Cannabinoid WIN 55,212-2 Sensitizes Hepatocellular Carcinoma Cells to Tumor Necrosis Factor-Related Apoptosis-Inducing Ligand (TRAIL)-I…

2010

In this article, we demonstrate that the synthetic cannabinoid R-(+)-(2,3-dihydro-5-methyl-3-[(4-morpholinyl)methyl]pyrol[1,2,3-de]-1,4-benzoxazin-6-yl)-(1-naphthalenyl) methanone mesylate (WIN 55,212-2) sensitizes human hepatocellular carcinoma (HCC) cells to apoptosis mediated by tumor necrosis-related apoptosis inducing ligand (TRAIL). The apoptotic mechanism induced by treatment with WIN/TRAIL combination involved the loss of the mitochondrial transmembrane potential and led to the activation of caspases. In HCC cells, WIN treatment induced the up-regulation of TRAIL death receptor DR5, an effect that seemed to be related to the increase in the level of p8 and CHOP, two factors implicat…

Carcinoma HepatocellularDNA ComplementaryMorpholinesApoptosisNaphthalenesCHOPMembrane PotentialsTNF-Related Apoptosis-Inducing LigandCell Line TumorSurvivinmedicineHumansWIN 55212-2Protein kinase BTranscription factorCaspaseDNA PrimersPharmacologybiologyCannabinoidsReverse Transcriptase Polymerase Chain ReactionLiver NeoplasmsGene AmplificationDNA NeoplasmFlow CytometryBenzoxazinesReceptors TNF-Related Apoptosis-Inducing LigandApoptosisMitochondrial MembranesImmunologybiology.proteinCancer researchMolecular MedicineTumor necrosis factor alphaTranscription Factor CHOPmedicine.drugMolecular Pharmacology
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Dynamics of Ca2+ and guanosine 5'-[gamma-thio]triphosphate action on insulin secretion from alpha-toxin-permeabilized HIT-T15 cells.

1994

The time course of Ca2+ and GTP-analogue effects on insulin secretion was investigated in HIT-T15 cells permeabilized with Staphylococcus alpha-toxin. These cells responded to Ca2+ in the range 0.1-10 microM and could be used in a dynamic perifusion system because of the minimal run-down of the secretory response. High Ca2+ (10 microM) elicited a monophasic ATP-dependent stimulation of insulin secretion that reached a peak within 5 min (approximately 20-fold increase) and rapidly decreased during the subsequent 15 min to a plateau remaining above basal rates (0.1 microM Ca2+). The decrease in Ca(2+)-induced insulin secretion with time could not be attributed to decreased capacity to respond…

Cell Membrane PermeabilityGTP'medicine.medical_treatmentStimulationCalcium-Calmodulin-Dependent Protein Kinases - antagonists & inhibitorsBiochemistryPiperazinesAdenosine TriphosphateDesensitization (telecommunications)1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineInsulin SecretionGuanosine 5'-O-(3-Thiotriphosphate) - pharmacologyStaphylococcus aureus alpha-toxinInsulinGuanosine Triphosphate - pharmacologyGuanylyl ImidodiphosphateKinasePiperazines - pharmacologyInsulin secretionAdenosine Triphosphate - pharmacologyPermeabilized cellsGuanosine TriphosphateResearch Articlemedicine.medical_specialtyStaphylococcus aureuschemistry.chemical_elementBiologyCalciumGuanylyl Imidodiphosphate - pharmacologyExocytosisCell LineInsulin - secretionInternal medicinemedicine1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine - analogs & derivativesSecretionMolecular BiologyInsulinCell BiologyIsoquinolinesATPKineticsEndocrinologyCalcium - pharmacologychemistryIsoquinolines - pharmacologyGuanosine 5'-O-(3-Thiotriphosphate)Type C PhospholipasesCalcium-Calmodulin-Dependent Protein KinasesCalciumType C Phospholipases - pharmacologyGTP
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Recent advances in the development of cyclin-dependent kinase 7 inhibitors.

2019

Abstract Cyclin dependent kinase 7 (CDK7) plays a double role as it activates several other cyclin dependent kinases and participates to the initiation of transcription. This kinase is overexpressed in various types of tumors. Relatively few selective CDK7 inhibitors have been up to now disclosed. Most of these inhibitors belong to two chemical families: pyrazolopyrimidines and pyrazolotriazines on one side and pyrimidines on another side. They also differ by their molecular mechanism of action. Some are acting as competitive inhibitors and some others are covalent inhibitors. With these tools, the understanding of the potential therapeutic interest of CDK7 inhibitors in cancer is rapidly g…

Cell SurvivalAntineoplastic Agents01 natural sciences03 medical and health sciencesDrug DevelopmentCyclin-dependent kinaseTranscription (biology)Cell Line TumorDrug DiscoverymedicineAnimalsHumansIC50Protein Kinase Inhibitors030304 developmental biologyPharmacology0303 health sciencesbiology010405 organic chemistryChemistryKinaseTriazinesOrganic ChemistryGeneral Medicinemedicine.diseaseCyclin-Dependent Kinases0104 chemical sciencesLeukemiaPyrimidinesbiology.proteinCancer researchMolecular mechanismCyclin-dependent kinase 7Cyclin-Dependent Kinase-Activating KinaseEuropean journal of medicinal chemistry
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Effect of L-Histidine on the Survival of a T-Strain of Mycoplasma

1975

The addition of L-histidine to the growth medium prolongs the stationary phase and the survival of a T-strain of mycoplasma. Results of an experiment performed with 14 C-labeled urea demonstrate that the action of L-histidine is based on the retardation of the rise of pH.

Cell SurvivalCell CountBuffersmedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyPiperazineschemistry.chemical_compoundHydrolysisMycoplasmamedicineUreaHistidineCarbon RadioisotopesGeneral Pharmacology Toxicology and PharmaceuticsCell survivalHistidineMetabolism and ProductsGrowth mediumGeneral Immunology and MicrobiologyStrain (chemistry)HydrolysisStereoisomerismGeneral MedicineMycoplasmaHydrogen-Ion ConcentrationMolecular biologychemistryBiochemistryStationary phaseUreaSulfonic Acids
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Cytotoxicity of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide in multidrug-resistant cancer cells through activation of PERK/eIF2α/AT…

2021

After decades of research, multidrug resistance (MDR) remains a huge challenge in cancer treatment. In this study, the cytotoxic of 4-hydroxy-N-(naphthalen-1-yl)-2-oxo-2H-chromene-3-carboxamide (MCC1734) has been investigated towards multidrug-resistant cancer cell lines. MCC1734 exerted cytotoxicity on cell lines expressing different mechanisms of drug resistance (P-glycoprotein, BCRP, ABCB5, EGFR, p53 knockout) to a different extent. Interestingly, sensitive CCRF-CEM cells and multidrug-resistant P-gp-overexpressing CEM/ADR5000 cells represented similar sensitivity towards MCC1734, indicating MCC1734 can bypass P-gp-mediated resistance. Microarray-based mRNA expression revealed that MCC17…

Cell SurvivalEukaryotic Initiation Factor-2Antineoplastic AgentsMitochondrionBiochemistryFlow cytometryeIF-2 KinaseCell Line TumorOxazinesmedicineHumansCytotoxic T cellGene Regulatory NetworksCytotoxicityPharmacologyMolecular Structuremedicine.diagnostic_testChemistryCell cycleActivating Transcription Factor 4Gene Expression Regulation NeoplasticXanthenesDrug Resistance NeoplasmCell cultureApoptosisCancer cellCancer researchGene DeletionBiochemical Pharmacology
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Electron microscopic demonstration of intracelluar promethazine accumulation sites by a precipitation technique: application to the cerebellar cortex…

1996

A method is described that allows electron microscopic identification of the phenothiazine neuroleptic promethazine after supravital intracardiac injection of high drug concentrations (greater than or equal to 3 %). The cerebellar cortex of the mouse was used for the investigation. This procedure is based on simultaneous fixation of drug and tissue by immersion in a paraformaldehyde-glutaraldehyde solution with the addition of phosphomolybdic acid. The electron microscopic investigation revealed that the drug could easily be identified as an electron-dense precipitate. Subpopulations of neurons exhibited a higher affinity for the drug than others, but no preference for any nerve cell type …

Cell typeTissue FixationHistologyChromatographyChemistryEndoplasmic reticulumMitochondrionPromethazinePromethazineCerebellar CortexMiceMicroscopy Electronchemistry.chemical_compoundCytoplasmCerebellar cortexPhenothiazineUltrastructureBiophysicsmedicineAnimalsAnatomymedicine.drugJournal of Histochemistry & Cytochemistry
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The Function of the Caudate Nucleus in the Control of Some Paroxystic Activities in the Neuraxis

1969

(1969). The Function of the Caudate Nucleus in the Control of Some Paroxystic Activities in the Neuraxis. Archives Internationales de Physiologie et de Biochimie: Vol. 77, No. 3, pp. 465-484.

Central Nervous SystemCerebral CortexPhysiologyCaudate nucleusStrychnineBiologyBiochemistryElectric StimulationElectrophysiologySpinal CordPyrazinesOxazinesCatsAnimalsPentylenetetrazolePicrotoxinCaudate NucleusNeuroscienceFunction (biology)Archives Internationales de Physiologie et de Biochimie
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