Search results for "kinases"

showing 10 items of 929 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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Aspidin PB, a phloroglucinol derivative, induces apoptosis in human hepatocarcinoma HepG2 cells by modulating PI3K/Akt/GSK3β pathway.

2012

Aspidin PB, a phloroglucinol derivative isolated from Dryopteris fragrans (L.) Schott, has been previously reported to exert high biological activities. In the present study, we analyzed the apoptotic mechanisms of aspidin PB on human hepatoma cell line, HepG2. Initially, aspidin PB was shown to inhibit the growth of HepG2 cells in a time and dose-dependent manner. After treatment with aspidin PB for 72 h, 48 h and 24 h using MTT assay, the IC(50) values were 10.59 μM, 20.86 μM and 46.59 μM, respectively. Aspidin PB was capable to induce apoptosis, as measured by mitochondrial membrane potential (ΔΨm), acridine orange (AO) staining and propidium iodide (PI)/annexin V-FITC double staining. T…

Carcinoma HepatocellularApoptosisBiologyPhloroglucinolToxicologyWortmanninchemistry.chemical_compoundGlycogen Synthase Kinase 3Phosphatidylinositol 3-KinasesAnnexinHumansMTT assayPropidium iodideProtein kinase BProtein Kinase InhibitorsPI3K/AKT/mTOR pathwayCell ProliferationPhosphoinositide-3 Kinase InhibitorsMembrane Potential MitochondrialGlycogen Synthase Kinase 3 betaMicroscopy ConfocalAcridine orangeLiver NeoplasmsGeneral MedicineHep G2 CellsFlow CytometryMolecular biologyAndrostadieneschemistryApoptosisWortmanninProto-Oncogene Proteins c-aktSignal TransductionChemico-biological interactions
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Supraventricular tachycardias, conduction disease, and cardiomyopathy in 3 families with the same rare variant in TNNI3K (p.Glu768Lys)

2018

IF 4.743 (2017); International audience; BackgroundRare genetic variants in TNNI3K encoding troponin-I interacting kinase have been linked to a distinct syndrome consisting primarily of supraventricular tachycardias and variably expressed conduction disturbance and dilated cardiomyopathy in 2 families.ObjectiveThe purpose of this study was to identify new genetic variants associated with inherited supraventricular tachycardias, cardiac conduction disease, and cardiomyopathy.MethodsWe conducted next generation sequencing in 3 independent multigenerational families with atrial/junctional tachycardia with or without conduction disturbance, dilated cardiomyopathy, and sudden death. We also asse…

Cardiomyopathy DilatedMaleKinaseAdolescentConduction diseaseBlotting WesternDNA Mutational AnalysisCardiomyopathyDilated cardiomyopathyMagnetic Resonance Imaging Cine030204 cardiovascular system & hematologyProtein Serine-Threonine KinasesSudden death03 medical and health sciencesYoung Adult0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemHeart Conduction SystemPhysiology (medical)Cardiac conductionmedicineTachycardia SupraventricularGeneticsHumans030212 general & internal medicineGenetic TestingKinase activityCells CulturedGeneticsbusiness.industryRare variantTNNI3KDilated cardiomyopathyDNAmedicine.diseasePedigreeProtein autophosphorylationSupraventricular tachycardiaJunctional tachycardiaMutationFemaleSupraventricular tachycardiaCardiology and Cardiovascular Medicinebusiness
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Deleting Full Length Titin Versus the Titin M-Band Region Leads to Differential Mechanosignaling and Cardiac Phenotypes

2019

Background: Titin is a giant elastic protein that spans the half-sarcomere from Z-disk to M-band. It acts as a molecular spring and mechanosensor and has been linked to striated muscle disease. The pathways that govern titin-dependent cardiac growth and contribute to disease are diverse and difficult to dissect. Methods: To study titin deficiency versus dysfunction, the authors generated and compared striated muscle specific knockouts (KOs) with progressive postnatal loss of the complete titin protein by removing exon 2 (E2-KO) or an M-band truncation that eliminates proper sarcomeric integration, but retains all other functional domains (M-band exon 1/2 [M1/2]-KO). The authors evaluated c…

Cardiomyopathy DilatedMaleSarcomeresanimal structuresVentricular Dysfunction Rightmacromolecular substances030204 cardiovascular system & hematologyMechanotransduction CellularVentricular Function LeftArticleMuscle hypertrophyVentricular Dysfunction Left03 medical and health sciences0302 clinical medicinePhysiology (medical)AnimalsMedicineMyocytes CardiacMuscle Skeletal030304 developmental biologyMice Knockout0303 health sciencesbiologybusiness.industryMolecular springmusculoskeletal systemPhenotypeCell biologyMuscular AtrophyPhenotypeMuscle diseasecardiovascular systemVentricular Function Rightbiology.proteinTitinCardiology and Cardiovascular MedicinebusinessProtein KinasesGene DeletionDifferential (mathematics)Circulation
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Synergistic Effect of Carfilzomib and Metformin in Vascular Plasticity; The Emerging Role of Autophagy

2019

Introduction: Carfilzomib (Cfz) correlates with a risk of reversible cardiotoxicity in 5-10% of multiple myeloma (MM) patients. We have recently shown that metformin (Met) has a prophylactic role against the Cfz-induced cardiotoxicity in vivo, through activation of AMPKα signaling (Blood 2019;133:710-23). However, the impact of Cfz on vascular function is obscure. Therefore, we sought to investigate: i) the acute, ii) the sub-chronic effect of Cfz on the vascular reactivity, iii) the effect of metformin co-administration on the vascular phenotype and iv) the impact of Cfz and Met co-administration on aged Human Aortic Smooth Muscle Cells (HAoSMCs). Methods: Forty male C57Bl/6 mice were assi…

CardiotoxicityMulticatalytic endopeptidase complexbusiness.industryMTOR Serine-Threonine KinasesImmunologyAutophagyCell BiologyHematologyBiochemistryCarfilzomibAngiotensin IIMetforminchemistry.chemical_compoundchemistryAnimals laboratoryCancer researchmedicinebusinessmedicine.drugBlood
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Transcriptional and post-transcriptional regulation of iNOS expression in human chondrocytes

2009

Chondrocytes are important for the development and maintenance of articular cartilage. However, both in osteoarthritis (OA) and rheumatoid arthritis (RA) chondrocytes are involved in the process of cartilage degradation and synthesize important immunomodulatory mediators, including nitric oxide (NO) generated by the inducible NO synthase (iNOS). To uncover the role of iNOS in the pathomechanisms of OA and RA, we analyzed the regulation of iNOS expression using immortalized human chondrocytes as a reproducible model. In C-28/I2 chondrocytes, iNOS expression was associated with the expression of the chondrocyte phenotype. Peak induction by a cytokine cocktail occurred between 6 and 8h and dec…

Cartilage Articularmedicine.medical_specialtyAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiologyBiochemistryp38 Mitogen-Activated Protein KinasesChondrocyteArticleGene Expression Regulation EnzymologicGlucocorticoid receptorChondrocytesReceptors GlucocorticoidInternal medicineGene expressionmedicineHumansRNA MessengerRNA Processing Post-TranscriptionalPost-transcriptional regulationCell Line TransformedPharmacologyRegulation of gene expressionNF-kappa B p50 SubunitRNA-Binding ProteinsInterferon-Stimulated Gene Factor 3Janus Kinase 2Cell biologyNitric oxide synthaseEndocrinologymedicine.anatomical_structureCell cultureEnzyme Inductionbiology.proteinTrans-ActivatorsCytokinesZearalenoneSignal transduction
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Cigarette Smoke Extract Induces p38 MAPK-Initiated, Fas-Mediated Eryptosis

2022

Eryptosis is a physiological mechanism for the clearance of senescent or damaged erythrocytes by phagocytes. Excessive eryptosis is stimulated under several pathologies and associated with endothelial injury and thrombosis. Cigarette smoke (CS) is an established risk factor for vascular diseases and cigarette smokers have high-levels of eryptotic erythrocytes. This study, for the first time, investigates the mechanism by which CS damages red blood cells (RBCs). CS extract (CSE) from commercial cigarettes was prepared and standardized for nicotine content. Cytofluorimetric analysis demonstrated that treatment of human RBCs with CSE caused dose-dependent, phosphatidylserine externalization an…

Caspase 8ErythrocytesCaspase 3cigarette smokeOrganic ChemistryGeneral Medicinep38 MAPKCeramidesp38 Mitogen-Activated Protein KinasesCatalysisComputer Science ApplicationsInorganic Chemistryeryptosis; cigarette smoke; death-inducing signaling complex (DISC); p38 MAPK; ceramide; caspasescaspasesSmokeeryptosisSettore BIO/10 - BiochimicaTobaccodeath-inducing signaling complex (DISC)HumansceramidePhysical and Theoretical ChemistryReactive Oxygen SpeciesMolecular BiologySpectroscopy
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Mechanisms of nitric-oxide-induced increase of free cytosolic Ca2+ concentration in Nicotiana plumbaginifolia cells.

2005

In this study, we investigated a role for nitric oxide (NO) in mediating the elevation of the free cytosolic Ca(2+) concentration ([Ca(2+)](cyt)) in plants using Nicotiana plumbaginifolia cells expressing the Ca(2+) reporter apoaequorin. Hyperosmotic stress induced a fast increase of [Ca(2+)](cyt) which was strongly reduced by pretreating cell suspensions with the NO scavenger carboxy PTIO, indicating that NO mediates [Ca(2+)](cyt) changes in plant cells challenged by abiotic stress. Accordingly, treatment of transgenic N. plumbaginifolia cells with the NO donor diethylamine NONOate was followed by a transient increase of [Ca(2+)](cyt) sensitive to plasma membrane Ca(2+) channel inhibitors …

Cations DivalentNicotiana tabacumAequorinNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundCytosolPhysiology (medical)medicineStaurosporinePhosphorylationProtein kinase ANicotiana plumbaginifoliaSolanaceaebiologyCell MembraneDepolarizationbiology.organism_classificationMolecular biologyMolecular WeightCytosolchemistryBiophysicsbiology.proteinCalciumProtein Kinasesmedicine.drugFree radical biologymedicine
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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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Quinoline-Based Molecules Targeting c-Met, EGF, and VEGF Receptors and the Proteins Involved in Related Carcinogenic Pathways

2020

The quinoline ring system has long been known as a versatile nucleus in the design and synthesis of biologically active compounds. Currently, more than one hundred quinoline compounds have been approved in therapy as antimicrobial, local anaesthetic, antipsychotic, and anticancer drugs. In drug discovery, indeed, over the last few years, an increase in the publication of papers and patents about quinoline derivatives possessing antiproliferative properties has been observed. This trend can be justified by the versatility and accessibility of the quinoline scaffold, from which new derivatives can be easily designed and synthesized. Within the numerous quinoline small molecules developed as a…

Cell SurvivalAngiogenesisPharmaceutical ScienceAntineoplastic AgentsReviewMolecular Dynamics SimulationAnalytical Chemistrylcsh:QD241-441Structure-Activity Relationship03 medical and health scienceschemistry.chemical_compound0302 clinical medicinelcsh:Organic chemistryEpidermal growth factorquinolineDrug DiscoverySAR studieHumansPhysical and Theoretical Chemistrycarcinogenic pathwaysProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biology0303 health sciencesantiproliferative compoundChemistryDrug discoveryOrganic ChemistryQuinolineBiological activityProto-Oncogene Proteins c-metantiproliferative compoundstargeted therapySettore CHIM/08 - Chimica FarmaceuticaSmall moleculeErbB Receptorscarcinogenic pathwayReceptors Vascular Endothelial Growth FactorSAR studiesChemistry (miscellaneous)030220 oncology & carcinogenesisQuinolinesCancer researchMolecular Medicinekinases modulatorkinases modulatorsbiological dataSignal TransductionMolecules
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