Search results for "Phosphorylation"

showing 10 items of 975 documents

In vivo and in vitro antioxidant properties of furosemide

2003

The aim of this study was to investigate in vivo and in vitro antioxidant properties of furosemide. In vitro, human red blood cells were submitted to oxidative stress (AAPH), in absence or in presence of different concentrations of furosemide. Potassium efflux was measured in order to quantify the oxidative stress after the action of AAPH on red blood cells. Allophycocyanin assay was also used to investigate antioxidant capacities of furosemide. For the in vivo experiment, male Wistar rats were used. A control group (n = 5) was treated by a daily intraperitoneal injection of saline solution (0.2 ml); 2 other groups (J0 and J+) were treated for 7 days by one daily intraperitoneal injection o…

MaleErythrocytesAntioxidantmedicine.medical_treatmentIntraperitoneal injectionAmidinesOxidative phosphorylationIn Vitro TechniquesPharmacologymedicine.disease_causeAntioxidantsGeneral Biochemistry Genetics and Molecular BiologyFurosemideIn vivomedicineAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsDiureticsSalineChemistryPhycocyaninFurosemideFree Radical ScavengersGeneral MedicineIn vitroRatsOxidative StressAnesthesiaPotassiumOxidative stressmedicine.drugLife Sciences
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Phospholipase D in rat myocardium: formation of lipid messengers and synergistic activation by G-protein and protein kinase C.

1998

Activation of phospholipase D (PLD) and phosphoinositide-specific phospholipase C (PI-PLC) by fluoride, to stimulate heterotrimeric G-proteins, and by phorbol esters, to stimulate protein kinase C (PKC), was studied in rat atria. Fluoride and 4beta-phorbol-12beta,13alpha-dibutyrate (PDB), in contrast to 4beta-phorbol-13alpha-acetate (PAc), activated PLD, catalyzing the formation of [3H]-phosphatidylethanol ([3H]-PETH), [3H]-phosphatidic acid ([3H]-PA), choline and sn-1,2-diacylglycerol (DAG). Basal PLD activity was resistant to drastic changes in Ca2+ and to Ro 31-8220, a PKC inhibitor, but was decreased by genistein, an inhibitor of tyrosine kinase, and increased by vanadate, a tyrosine ph…

MaleG proteinProtein tyrosine phosphataseBiologyBiochemistrySecond Messenger Systemschemistry.chemical_compoundPhosphoinositide Phospholipase CGTP-Binding ProteinsPhorbol EstersPhospholipase DAnimalsRats WistarProtein kinase CPhorbol 1213-DibutyrateProtein Kinase CDiacylglycerol kinasePharmacologyPhospholipase CPhospholipase DMyocardiumPhosphatidylinositol Diacylglycerol-LyaseTyrosine phosphorylationDrug SynergismLipid MetabolismLipidsRatsEnzyme ActivationBiochemistrychemistryType C PhospholipasesSecond messenger systemlipids (amino acids peptides and proteins)Biochemical pharmacology
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Silibinin improves hepatic and myocardial injury in mice with nonalcoholic steatohepatitis

2012

Abstract Background Nonalcoholic fatty liver disease is a chronic metabolic disorder with significant impact on cardiovascular and liver mortality. Aims In this study, we examined the effects of silibinin on liver and myocardium injury in an experimental model of nonalcoholic fatty liver disease. Methods A four-week daily dose of silibinin (20 mg/kg i.p.) was administrated to db/db mice fed a methionine–choline deficient diet. Hepatic and myocardial histology, oxidative stress and inflammatory cytokines were evaluated. Results Silibinin administration decreased HOMA-IR, serum ALT and markedly improved hepatic and myocardial damage. Silibinin reduced isoprostanes, 8-deoxyguanosine and nitrit…

MaleGene ExpressionIsoprostanesmedicine.disease_causeGastroenterologyAntioxidantsMicechemistry.chemical_compoundMethionineNon-alcoholic Fatty Liver DiseaseNonalcoholic fatty liver diseasePhosphorylationGastroenterologyAlanine TransaminaseGlutathioneCholine DeficiencyMitochondrial respiratory chainLiverHeart Inflammation NAFLD Oxidative stress SilibininCytokinesmedicine.symptomSilymarinmedicine.medical_specialtySilibininInflammationStatistics NonparametricProinflammatory cytokineInsulin resistanceInternal medicinemedicineAnimalsNitritesAnalysis of VarianceNitratesHepatologySettore BIO/16 - Anatomia Umanabusiness.industryMyocardiumJNK Mitogen-Activated Protein KinasesGlutathionemedicine.diseaseDietFatty LiverOxidative StressEndocrinologychemistrySilybinInsulin ResistancebusinessOxidative stressDigestive and Liver Disease
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Anti-inflammatory and antioxidant effects of muscarinic acetylcholine receptor (mAChR) activation in the rat hippocampus

2019

AbstractRecently we found that acute treatment with Oxotremorine (Oxo), a non-selective mAChRs agonist, up-regulates heat shock proteins and activates their transcription factor heat shock factor 1 in the rat hippocampus. Here we aimed to investigate: a) if acute treatment with Oxo may regulate pro-inflammatory or anti-inflammatory cytokines and oxidative stress in the rat hippocampus; b) if chronic restraint stress (CRS) induces inflammatory or oxidative alterations in the hippocampus and whether such alterations may be affected by chronic treatment with Oxo. In the acute experiment, rats were injected with single dose of Oxo (0.4 mg/kg) and sacrificed at 24 h, 48 h and 72 h. In the CRS ex…

MaleHydrocortisonemedicine.medical_treatmentInterleukin-1betaNeuroimmunologyAnti-Inflammatory Agentslcsh:MedicinePharmacologymedicine.disease_causeHippocampusSettore BIO/09 - FisiologiaAntioxidantsSuperoxide Dismutase-1Muscarinic acetylcholine receptorPhosphorylationlcsh:Sciencechemistry.chemical_classificationMultidisciplinarybiologyneurodegenerationAlzheimer's diseaseReceptors MuscarinicNeuroprotective AgentsCytokineSignal Transductionmedicine.drugRestraint PhysicalAgonistmedicine.drug_classScopolaminemuscarinic acetylcholine receptorMuscarinic AgonistsArticleOxotremorine anti-inflammatory cytokinesSuperoxide dismutaseHeat shock proteinOxotremorinemedicineAnimalsRats WistarInflammationReactive oxygen speciesInterleukin-6Superoxide DismutaseOxotremorinelcsh:RTranscription Factor RelARatsOxidative Stresschemistrybiology.proteinlcsh:QReactive Oxygen SpeciesProtein Processing Post-TranslationalOxidative stressScientific Reports
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Combined hyperthermia and chlorophyll-based photodynamic therapy: tumour growth and metabolic microenvironment

2003

The effects of combined and simultaneously applied localised 43 degrees C hyperthermia (HT) and an antivascular bacteriochlorophyll-serine-based photodynamic therapy (Bchl-ser-PDT) on tumour growth and several microenvironmental parameters were examined. Rats bearing DS-sarcomas were allocated to treatment groups: (i) sham-treatment (control), (ii) Bchl-ser-PDT (20 mg kg(-1) i.v.), (iii) localised HT, (iv) Bchl-ser-PDT+HT. The light source used was an infrared-A irradiator, which, by use of appropriate filters, delivered the different ranges of wavelengths required. Following treatment, tumour volume was monitored. The greatest tumour growth inhibition was seen with Bchl-ser-PDT+HT, and sub…

MaleHyperthermiaCancer ResearchPathologymedicine.medical_specialtymedicine.medical_treatmentAngiogenesis InhibitorsPhotodynamic therapyOxidative phosphorylationBiologyPharmacologyRats Sprague-DawleyNeovascularizationchemistry.chemical_compoundmedicineAnimalsblood flowCombined Modality TherapyGlycolysisExperimental TherapeuticBacteriochlorophyllsPhotosensitizing AgentsNeovascularization PathologicbacteriochlorophyllHyperthermia InducedOxygenationhyperthermiamedicine.diseaseCombined Modality TherapyCell Hypoxiametabolic statusRatsPhotochemotherapyphotodynamic therapyOncologychemistryModels AnimalSarcoma ExperimentaloxygenationGrowth inhibitionmedicine.symptomCell DivisionBritish Journal of Cancer
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Gitelman-Like Syndrome Caused by Pathogenic Variants in mtDNA

2022

Contains fulltext : 248375.pdf (Publisher’s version ) (Closed access) BACKGROUND: Gitelman syndrome is the most frequent hereditary salt-losing tubulopathy characterized by hypokalemic alkalosis and hypomagnesemia. Gitelman syndrome is caused by biallelic pathogenic variants in SLC12A3, encoding the Na(+)-Cl(-) cotransporter (NCC) expressed in the distal convoluted tubule. Pathogenic variants of CLCNKB, HNF1B, FXYD2, or KCNJ10 may result in the same renal phenotype of Gitelman syndrome, as they can lead to reduced NCC activity. For approximately 10 percent of patients with a Gitelman syndrome phenotype, the genotype is unknown. METHODS: We identified mitochondrial DNA (mtDNA) variants in th…

MaleKidneyDISEASEion transportGenotypeSolute Carrier Family 12 Member 3Gitelman-s syndromeCHANNEL GENEChildRNA Transfer IlePHOSPHORYLATIONNCCbiologygenetic renal diseaseblood pressureMetabolic Disorders Radboud Institute for Molecular Life Sciences [Radboudumc 6]General MedicineMiddle Agedchronic kidney failureTUBULENa transportPedigreemitochondriaBARTTER-SYNDROMEPhenotypemedicine.anatomical_structureMitochondrial respiratory chainMAGNESIUMNephrologyChild Preschoolepithelial sodium transportFemaleGitelman SyndromeAdultMitochondrial DNAAdolescentGenotypehuman geneticsKCNJ10DNA MitochondrialModels BiologicalPolymorphism Single NucleotideRNA Transfer PheYoung AdultTubulopathymedicineHumansDistal convoluted tubuleHYPOMAGNESEMIAAgedCLCNKBNeurodevelopmental disorders Donders Center for Medical Neuroscience [Radboudumc 7]MITOCHONDRIAL-DNA MUTATIONBase SequenceInfantGitelman syndromemedicine.diseaseMolecular biologySODIUM-CHLORIDE COTRANSPORTERHEK293 CellsRenal disorders Radboud Institute for Molecular Life Sciences [Radboudumc 11]Basic ResearchMutationbiology.proteinNucleic Acid Conformationchronic kidney disease
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Detection of increased tyrosine phosphorylation in murine Langerhans cells after stimulation with contact sensitizers.

1999

The signalling pathways in epidermal Langerhans cells (LC) during activation by contact sensitizers are poorly understood. Recently, we have described an increased phosphorylation of tyrosine residues in human MHC class II-positive cells in vitro following stimulation with contact sensitizers. In the study reported here the formation of phosphotyrosine (p-tyr) in murine epidermal LC upon stimulation with contact sensitizers was examined. By the use of a flow cytometric technique a significant increase in p-tyr was demonstrated in LC stimulated in vitro with the strong contact sensitizers TNCB (2,4,6-trinitro-chlorobenzene) and MCI/MI (5-chloro-2-methylisothiazolinone plus 2-methylisothiazol…

MaleLangerhans cellBlotting WesternDermatologyPicryl ChlorideBiologyCell Linechemistry.chemical_compoundMicemedicineAnimalsTyrosinePhosphorylationPhosphotyrosineMice Inbred BALB CTyrosine phosphorylationGeneral MedicineDendritic cellFlow CytometryMolecular biologyIn vitromedicine.anatomical_structureBiochemistrychemistryLangerhans CellsPhosphorylationTyrosineFemaleTyrphostin A9Signal transductionSignal TransductionArchives of dermatological research
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Inflammation-Induced Alteration of Astrocyte Mitochondrial Dynamics Requires Autophagy for Mitochondrial Network Maintenance

2013

Accumulating evidence suggests that changes in the metabolic signature of astrocytes underlie their response to neuroinflammation, but how proinflammatory stimuli induce these changes is poorly understood. By monitoring astrocytes following acute cortical injury, we identified a differential and region-specific remodeling of their mitochondrial network: while astrocytes within the penumbra of the lesion undergo mitochondrial elongation, those located in the core-the area invaded by proinflammatory cells-experience transient mitochondrial fragmentation. In brain slices, proinflammatory stimuli reproduced localized changes in mitochondrial dynamics, favoring fission over fusion. This effect w…

MaleLipopolysaccharidesPhysiologyDnm1l protein mouseInterleukin-1betaNitric Oxide Synthase Type IIMitochondrionAstrocytes/metabolismMitochondrial DynamicsAutophagy-Related Protein 7Mice0302 clinical medicinemetabolism [Reactive Oxygen Species]PhosphorylationCells Culturedcytology [Astrocytes]0303 health sciencesmetabolism [Inflammation]metabolism [Astrocytes]Inflammation/metabolismCytokines/metabolismdrug effects [Mitochondria]Mitochondria/drug effectsMitochondriaCell biologyAstrocytes/drug effectsmedicine.anatomical_structureMicrotubule-Associated Proteins/metabolismPhosphorylationCytokinesmetabolism [Dynamins]Nitric Oxide Synthase Type II/metabolismMicrotubule-Associated ProteinsAstrocytegenetics [Microtubule-Associated Proteins]DynaminsProgrammed cell deathAstrocytes/cytologydrug effects [Astrocytes]Mice TransgenicBiologypharmacology [Interferon-gamma]Proinflammatory cytokine03 medical and health sciencesInterferon-gammametabolism [Interleukin-1beta]reactive astrocytesReactive Oxygen Species/metabolismddc:570Mitochondria/metabolismtoxicity [Lipopolysaccharides]medicineAutophagyAnimalsAutophagy-Related Protein 7Molecular BiologyNeuroinflammation030304 developmental biologypathology [Inflammation]Dynamins/metabolismInflammationdrug effects [Mitochondrial Dynamics]Autophagymetabolism [Cytokines]Interferon-gamma/pharmacologyCell Biologymetabolism [Microtubule-Associated Proteins]Microtubule-Associated Proteins/geneticsMitochondrial Dynamics/drug effectsmetabolism [Mitochondria]metabolism [Nitric Oxide Synthase Type II]Mice Inbred C57BLLipopolysaccharides/toxicityAtg7 protein mouseAstrocytesInterleukin-1beta/metabolismReactive Oxygen Species030217 neurology & neurosurgeryInflammation/pathologyCell Metabolism
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PBDEs affect inflammatory and oncosuppressive mechanisms via the EZH2 methyltransferase in airway epithelial cells

2021

Abstract Aims We aimed to investigate the effect of PBDEs (47, 99, 209) on cellular events involved in epigenetic modification, inflammation, and epithelial mesenchymal transition (EMT). Materials and methods We studied: 1) ERK1/2 phosphorylation; 2) Enhancer of Zester Homolog 2 (EZH2); 3) Histone H3 tri-methylated in lysine 27 (H3K27me3); 4) K-RAS; 5) silencing disabled homolog 2-interacting protein gene (DAB2IP), 6) let-7a; 7) Muc5AC/Muc5B, and 8) IL-8 in a 3D in vitro model of epithelium obtained with primary Normal Human Bronchial Epithelial cells (pNHBEs) or A549 cell line, chronically exposed to PBDEs (47, 99, 209). Key findings PBDEs (10 nM, 100 nM and 1 μM) increased ERK1/2 phosphor…

MaleLung NeoplasmsMethyltransferaseRespiratory Mucosamacromolecular substancesAirway epithelial cellsGeneral Biochemistry Genetics and Molecular BiologyHistone H3Airway epithelial cellHalogenated Diphenyl EthersPolybrominated diphenyl ethersHumansGene silencingEnhancer of Zeste Homolog 2 ProteinEpigeneticsEpithelial–mesenchymal transitionGeneral Pharmacology Toxicology and PharmaceuticsProtein gene (DAB2IP)AgedFlame RetardantsInflammationA549 cellChemistryEZH2Epithelial CellsLet-7aGeneral MedicineMiddle AgedNeoplasm ProteinsA549 CellsCancer researchDisabled homolog 2 interactingPhosphorylationFemaleLung cancerLife Sciences
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Roles of the Raf/MEK/ERK and PI3K/PTEN/Akt/mtor pathways in controlling growth and sensitivity to therapy-implications for cancer and aging

2011

Dysregulated signaling through the Ras/Raf/MEK/ERK and PI3K/PTEN/Akt/mTOR pathways is often the result of genetic alterations in critical components in these pathways or upstream activators. Unrestricted cellular proliferation and decreased sensitivity to apoptotic-inducing agents are typically associated with activation of these pro-survival pathways. This review discusses the functions these pathways have in normal and neoplastic tissue growth and how they contribute to resistance to apoptotic stimuli. Crosstalk and commonly identified mutations that occur within these pathways that contribute to abnormal activation and cancer growth will also be addressed. Finally the recently described …

MaleMAPK/ERK pathwayAgingMAP Kinase Signaling SystemCancer aging RAF MEK mTORApoptosisReviewBiologyPI3KModels BiologicalApoptosis; Cancer; Kinases; MEK; MTOR; PI3K; Protein phosphorylation; RAF; Signal transductionMicePhosphatidylinositol 3-Kinases03 medical and health sciences0302 clinical medicineCancer stem cellNeoplasmscancerAnimalsHumansPTENProtein kinase BCellular SenescencePI3K/AKT/mTOR pathwayCell Proliferation030304 developmental biology0303 health sciencesKinaseTOR Serine-Threonine KinasesapoptosisPTEN PhosphohydrolaseRafCell BiologyMEKprotein phosphorylation3. Good healthCell biologyCrosstalk (biology)kinases030220 oncology & carcinogenesisMutationmTORCancer researchbiology.proteinFemaleraf KinasesProto-Oncogene Proteins c-aktCell agingsignal transduction
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