Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

Depletion of tumour glutathione in vivo by buthionine sulphoximine: modulation by the rate of cellular proliferation and inhibition of cancer growth.

1993

We have investigated in Ehrlich-ascites-tumour-bearing mice the effect of buthionine sulphoximine (BSO), a selective inhibitor of GSH synthesis, on the rate of GSH depletion of tumour versus normal tissues and its relation to tumour cell proliferation. In normal tissues, GSH and GSSG remain unchanged or close to normal values during tumour growth, even at the last stage of growth when the animal is close to death. After administration of a single dose of BSO (4 mmol/kg), the rates of GSH depletion and recovery in the tumour and in several normal tissues are very different. BSO depletes GSH in cancer cells to a level of 0.3-0.4 mumol/g. The fall in GSH levels is faster when tumour cells do n…

MaleAntimetabolites AntineoplasticIntracellular pHPharmacologyBiologyBiochemistrychemistry.chemical_compoundMiceIn vivoMethionine SulfoximineAnimalsButhionine sulfoximineCarcinoma Ehrlich TumorMolecular BiologyButhionine SulfoximineProtein kinase CDose-Response Relationship DrugCell growthCell BiologyGlutathioneGlutathioneDose–response relationshipchemistryBiochemistryCancer cellCell DivisionResearch Article
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Effect of gender on mitochondrial toxicity of Alzheimer's Abeta peptide.

2007

The aim of this article is to review the role of mitochondria in the pathogenesis of Alzheimer's disease. Additionally, the effect of gender on the incidence of Alzheimer's disease and the pathophysiological mechanisms involved will be discussed. Mitochondria, in the presence of Alzheimer's amyloid-beta peptide, increase the formation of reactive oxygen species which act both as damaging agents and also as signaling molecules. These radicals, in fact, unleash a mechanism involving the liberation of cytochrome c that leads to neuronal apoptosis. Notably, young females appear protected against the mitochondrial toxicity of amyloid-beta, likely due to the upregulation of antioxidant enzymes wh…

MaleAntioxidantPhysiologymedicine.medical_treatmentClinical BiochemistryPharmacologyMitochondrionBiologymedicine.disease_causeBiochemistryp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundDownregulation and upregulationAlzheimer DiseasemedicineHumansMolecular BiologyGeneral Environmental Sciencechemistry.chemical_classificationReactive oxygen speciesAmyloid beta-PeptidesEstrogensCell Biologymedicine.diseaseOxidantsMitochondriaEnzyme ActivationMitochondrial toxicitychemistryBiochemistryToxicityGeneral Earth and Planetary SciencesPhytoestrogensFemaleOxidative stressAntioxidantsredox signaling
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Activation of L-arginine transport by protein kinase C in rabbit, rat and mouse alveolar macrophages

1998

1 The role of protein kinase C in controlling L-arginine transport in alveolar macrophages was investigated. 2 L-[3H]Arginine uptake in rabbit alveolar macrophages declined by 80 % after 20 h in culture. 4β-Phorbol 12-myristate 13-acetate (PMA), but not 4α-phorbol 12-myristate 13-acetate (α-PMA), present during 20 h culture, enhanced L-[3H]arginine uptake more than 10-fold. Staurosporine and chelerythrine opposed this effect. 3 L-[3H]Arginine uptake was saturable and blockable by L-lysine. After PMA treatment Vmax was increased more than 5-fold and Km was reduced from 0.65 to 0.32 mM. 4 Time course experiments showed that PMA increased L-[3H]arginine uptake almost maximally within 2 h. This…

MaleArgininePhysiologyMice Inbred StrainsStimulationCycloheximideArginineTritiumL-arginine transportRats Sprague-DawleyMicechemistry.chemical_compoundSpecies SpecificityLeucineMacrophages AlveolarmedicineAnimalsStaurosporineRNA MessengerEnzyme InhibitorsProtein Kinase CProtein kinase CbiologySodiumMembrane ProteinsBiological TransportRabbit ratOriginal Articlesbiology.organism_classificationMolecular biologyRatsKineticsChelerythrinechemistryEthylmaleimideCarcinogensAmino Acid Transport Systems BasicTetradecanoylphorbol AcetateFemaleRabbitsCarrier Proteinsmedicine.drugThe Journal of Physiology
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Vitamin E activates CRABP-II gene expression in cultured human fibroblasts, role of protein kinase C

2004

The treatment of human fibroblasts with different tocopherols in the presence of retinol caused an increase in cytoplasmic retinoic acid binding protein II (CRABP-II) mRNA and protein. The possibility of an involvement of protein kinase C (PKC) in the response to tocopherols was supported by the results obtained with the PKC-specific inhibitors, calphostin C and bisindolylmaleimide I. The effect of alpha-tocopherol was prevented by okadaic acid, suggesting that a protein phosphatase is responsible for PKC dephosphorylation produced by the presence of tocopherols. The results shown support the hypothesis that phosphorylation/dephosphorylation of RXRalpha via PKC may be involved in the regula…

MaleBisindolylmaleimideTranscription GeneticReceptors Retinoic AcidPhosphatasealpha-TocopherolBiophysicsBiochemistryDephosphorylationchemistry.chemical_compoundStructural BiologyProtein kinase COkadaic AcidGeneticsHumansVitamin ERNA MessengerRetinoic acid bindingPhosphorylationMolecular BiologyProtein kinase CCells CulturedDNA PrimersBase SequenceReverse Transcriptase Polymerase Chain ReactionInfant NewbornRetinoid X receptor αCell BiologyMolecular biologyRetinoic acid receptorCalphostin CchemistryGene Expression RegulationProtein phosphatasePhosphorylationFibroblastCytoplasmic retinoic acid binding protein IIFEBS Letters
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TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
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Midostaurin upregulates eNOS gene expression and preserves eNOS function in the microcirculation of the mouse

2005

Nitric oxide (NO) derived from endothelial NO synthase (eNOS) is a powerful vasodilator and possesses vasoprotective effects. Therefore, augmentation of eNOS expression and -activity by pharmacological means could provide protection against cardiovascular disease. However, this concept has been questioned recently, because in several disease models, eNOS upregulation was associated with a dysfunctional enzyme (referred to as eNOS uncoupling). In contrast, the present study demonstrates that an eNOS gene expression-enhancing compound with additional protein kinase C (PKC) inhibitory properties can upregulate eNOS while preserving its enzymatic function. Apolipoprotein E-knockout mice were tr…

MaleCancer ResearchNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryNitric Oxide Synthase Type IIBiologyPharmacologyBiochemistryNitric oxideMicechemistry.chemical_compoundApolipoproteins EEnosmedicineAnimalsStaurosporineRNA MessengerMidostaurinAortaNitritesProtein kinase CMice KnockoutNitratesMicrocirculationStaurosporinebiology.organism_classificationVasoprotectiveVasodilationNitric oxide synthaseBiochemistrychemistryEnzyme Inductionbiology.proteinNitric Oxide SynthaseReactive Oxygen SpeciesIntravital microscopymedicine.drugNitric Oxide
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cAMP-dependent phosphorylation of CYP2B1 as a functional switch for cyclophosphamide activation and its hormonal controlin vitro andin vivo

2001

An important feature of cytochrome P450 (CYP) 2B1 is its high ability to convert the prodrug cyclophosphamide (CPA) to therapeutically cytotoxic metabolites, resulting in interstrand DNA-cross-linking and cell death. We have examined whether and how the phosphorylation of CYP2B1 influences CPA metabolic activation in vitro and in vivo. We found first that only part of the total CYP2B1 pool undergoes phosphorylation. This part is fully inactivated. Second, phosphorylation of CYP2B1 in intact hepatocytes reduced by up to 75% toxification of CPA to mutagenic metabolites (totally dependent on the same preferentially CYP2B-catalyzed 4-hydroxylation of CPA as is the generation of highly cytotoxic…

MaleCancer ResearchProgrammed cell deathTime FactorsCellRats Sprague-DawleyStructure-Activity RelationshipSex FactorsIn vivoCyclic AMPPhosphoprotein PhosphatasesSerinemedicineAnimalsCytotoxic T cellheterocyclic compoundsPhosphorylationProtein kinase AAntineoplastic Agents AlkylatingCyclophosphamideBiotransformationbiologyCytochrome P450GlucagonCyclic AMP-Dependent Protein KinasesIn vitroRatsCell biologymedicine.anatomical_structureOncologyBiochemistryCytochrome P-450 CYP2B1Hepatocytescardiovascular systembiology.proteinPhosphorylationFemaleMutagensInternational Journal of Cancer
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Trastuzumab therapy vs tetracycline controlled ERBB2 downregulation: influence on tumour development in an ERBB2-dependent mouse tumour model

2008

Trastuzumab (Herceptin) has improved therapy of breast cancer. Only patients overexpressing ERBB2 are treated with trastuzumab, whereas its use in tumours without ERBB2 expression is useless. This led to the concept that the subgroup of trastuzumab-sensitive tumours is ‘ERBB2-dependent', meaning that ERBB2 signalling is indispensable for growth of these tumours. We used a mouse model that allows anhydrotetracycline (ATc)-controlled downregulation of ERBB2 in tumour tissue. ERBB2 mRNA and protein expression were downregulated below detection limit leading to a macroscopically complete tumour remission within 14 days. Tumour remission was accompanied by a strong decrease in proliferation, a m…

MaleCancer ResearchReceptor ErbB-2AKT1AKT2ApoptosisMiceTrastuzumabPKBskin and connective tissue diseasesERBB2Mitogen-Activated Protein Kinase 3biologyERK1/2herceptinAntibodies MonoclonalCytochromes cImmunohistochemistrynude miceGene Expression Regulation NeoplasticOncologyTetracyclinesKi-67Ki-67Femalemedicine.drugmedicine.medical_specialtyBlotting WesternDown-RegulationMice NudeAntineoplastic AgentsProtein Serine-Threonine KinasesAntibodies Monoclonal Humanizedresistance3-Phosphoinositide-Dependent Protein Kinasesbreast cancerDownregulation and upregulationresponse to therapyInternal medicineHER2medicineAnimalsRNA Messengercytochrome c releaseProtein kinase Bneoplasmstumour developmentCell Proliferationhumanised monoclonal antibodyAktCancerMammary Neoplasms ExperimentalTrastuzumabmedicine.diseaseEndocrinologyKi-67 AntigenApoptosisDrug Resistance Neoplasmbiology.proteinCancer researchreceptor tyrosine kinaseTranslational TherapeuticsProto-Oncogene Proteins c-aktBritish Journal of Cancer
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Cardiovascular Toxicity in Cancer Patients Treated with Tyrosine Kinase Inhibitors: A Real-World Single-Center Experience

2019

<b><i>Background:</i></b> Target therapy can cause various cardiovascular complications. The aim of this study was to evaluate the burden of cardiovascular complications related to treatment with anti-BCR-ABL tyrosine kinase inhibitors (TKIs) and to determine if there are differences between the latest- and first-generation TKIs. <b><i>Methods:</i></b> A retrospective observational study was carried out on 55 patients (39 men, 16 women; mean age ± SD: 58 ± 11 years) treated with TKIs targeting Bcr-Abl for a median period of 3.5 years. Patients were divided in two groups according to the type of treatment. Group A included patients treated with…

MaleCancer Researchmedicine.medical_specialtyGastrointestinal Stromal TumorsDasatinibFusion Proteins bcr-ablCoronary Artery DiseasePulse Wave AnalysisCardio-oncology Cardiotoxicity Tyrosine kinase inhibitors Chronic myeloid leukemia Arterial stiffness03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineLeukemia Myelogenous Chronic BCR-ABL PositiveMedicineHumans030212 general & internal medicineAdverse effectPulse wave velocityProtein Kinase InhibitorsAgedGastrointestinal NeoplasmsRetrospective Studiesbusiness.industryPonatinibImidazolesRetrospective cohort studyGeneral MedicineMiddle Agedmedicine.diseaseThrombosisrespiratory tract diseasesDasatinibPyridazinesPyrimidinesTreatment OutcomeOncologyNilotinibchemistry030220 oncology & carcinogenesisArterial stiffnessCardiologyImatinib MesylateFemalebusinessmedicine.drugFollow-Up Studies
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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