Search results for "Enzyme Activation"

showing 10 items of 304 documents

Apoptosis induced in vascular smooth muscle cells by oxidative stress is partly prevented by pretreatment with CGRP.

2003

MAPK/ERK pathwaymedicine.medical_specialtyVascular smooth muscleMitogen-Activated Protein Kinase 3Calcitonin Gene-Related PeptideNeuropeptideApoptosisCalcitonin gene-related peptidemedicine.disease_causeGeneral Biochemistry Genetics and Molecular BiologyMuscle Smooth VascularHistory and Philosophy of ScienceInternal medicinemedicine.arterymedicineAnimalsRats WistarAortaCells CulturedMitogen-Activated Protein Kinase 1AortaMitogen-Activated Protein Kinase 3ChemistryGeneral NeuroscienceRatsEnzyme ActivationOxidative StressEndocrinologyApoptosisMitogen-Activated Protein KinasesOxidative stressAnnals of the New York Academy of Sciences
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Activation of MAP kinase signaling pathway in the mussel Mytilus galloprovincialis as biomarker of environmental pollution

2010

Stimulation of MAP kinase signal transduction pathway by various stressful stimuli was investigated in the marine bivalve Mytilus galloprovincialis. Analyses were performed in animals exposed in laboratory to selected pollutants and in mussels collected in winter and summer along the eastern Adriatic coast (Croatia). Effects of oxidative stress, induced by tributyltin, hydrogen peroxide and water soluble fraction of diesel fuel on the activation/phosphorylation of the three Mitogen-Activated Protein Kinases (MAPKs) p38, JNK and ERK using a newly developed ELISA procedure were evaluated. MAP kinase activation was analyzed 1 h after exposure of mussels to chemical agents, and after recovery p…

MAPK/ERK pathwaymussel Mytilus galloprovincialisMAP Kinase Kinase 4MAP Kinase Signaling SystemHealth Toxicology and Mutagenesisp38 mitogen-activated protein kinasesEnvironmental pollutionEnzyme-Linked Immunosorbent Assaypollution ; biomarker ; MAP kinase ; mussel ; Mytilus galloprovincialis ; tributyltin ; diesel oil ; hydrogen peroxide010501 environmental sciencesAquatic Science01 natural sciencesp38 Mitogen-Activated Protein Kinases03 medical and health scienceschemistry.chemical_compoundAnimals14. Life underwaterExtracellular Signal-Regulated MAP Kinases030304 developmental biology0105 earth and related environmental sciencesMytilus0303 health sciencesbiologyKinaseMusselHydrogen Peroxidebiology.organism_classificationMytilusCell biologyEnzyme Activationchemistry13. Climate actionEnvironmental chemistryMitogen-activated protein kinaseTributyltinbiology.proteinbiomarkerMAP kinaseMitogen-Activated Protein KinasesTrialkyltin Compoundsenvironmental pollutionBiomarkersGasolineWater Pollutants Chemical
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Trefoil factor TFF1-induced protection of conjunctival cells from apoptosis at premitochondrial and postmitochondrial levels.

2008

PURPOSE. Goblet cells of the conjunctival epithelium synthesize and secrete TFF1 (Trefoil factor 1), a small protease-resistant peptide that, together with mucins, is responsible for the rheologic properties of the tear film. This study aimed to determine whether TFF1, whose synthesis increases in inflammatory conditions such as pterygium, could protect conjunctival cells from apoptosis. METHODS. Chang conjunctival cells, either wild-type or expressing TFF1 through stable transfection, were exposed to benzalkonium chloride (BAK) and ultraviolet (UV) irradiation to trigger apoptosis. The authors used cell fractionation to detect lipid raft‐associated proteins, coimmunoprecipitation to explor…

MESH : Cell LineMESH : Chromosomes Human Pair 21Chromosomes Human Pair 21CellApoptosisMESH: Flow CytometryMESH: Caspase 8Membrane Potentials0302 clinical medicineMESH: Mitochondrial MembranesMESH: Chromosomes Human Pair 21MESH : Membrane Potentials0303 health sciencesCaspase 8MESH : Caspase 8MESH : Benzalkonium CompoundsMESH : Tumor Suppressor ProteinsChromosome MappingFas receptorFlow CytometryXIAPMitochondriaMESH : Epithelial Cellsmedicine.anatomical_structureMESH: Epithelial Cells030220 oncology & carcinogenesisMitochondrial MembranesTrefoil Factor-1MESH : MitochondriaMESH : TransfectionBenzalkonium CompoundsConjunctivaMESH: Benzalkonium CompoundsProgrammed cell deathMESH: Enzyme ActivationMESH : ConjunctivaUltraviolet RaysMESH : Flow CytometryMESH: MitochondriaMESH: ConjunctivaCaspase 3BiologyInhibitor of apoptosisCaspase 8TransfectionCell Line03 medical and health sciencesMESH : Mitochondrial Membranesmedicine[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular BiologyHumansMESH: Membrane PotentialsMESH: Tumor Suppressor Proteins[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH: HumansTumor Suppressor ProteinsMESH: ApoptosisMESH: TransfectionMESH : HumansEpithelial CellsMolecular biologyMESH: Cell LineEnzyme ActivationApoptosisMESH : Ultraviolet RaysMESH: Ultraviolet RaysMESH : Enzyme ActivationMESH: Chromosome MappingMESH : ApoptosisMESH : Chromosome Mapping
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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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Colony-stimulating factor-1-induced oscillations in phosphatidylinositol-3 kinase/AKT are required for caspase activation in monocytes undergoing dif…

2009

Abstract The differentiation of human peripheral blood monocytes into resident macrophages is driven by colony-stimulating factor-1 (CSF-1), which upon interaction with CSF-1 receptor (CSF-1R) induces within minutes the phosphorylation of its cytoplasmic tyrosine residues and the activation of multiple signaling complexes. Caspase-8 and -3 are activated at day 2 to 3 and contribute to macrophage differentiation, for example, through cleavage of nucleophosmin. Here, we show that the phosphatidylinositol-3 kinase and the downstream serine/threonine kinase AKT connect CSF-1R activation to caspase-8 cleavage. Most importantly, we demonstrate that successive waves of AKT activation with increasi…

Macrophage colony-stimulating factorCellular differentiationImmunologyImmunoblottingApoptosisBiologyBiochemistryMonocytesImmunoenzyme TechniquesPhosphatidylinositol 3-KinasesHumansImmunoprecipitationRNA MessengerPhosphorylationProtein kinase BCells CulturedPhosphoinositide-3 Kinase InhibitorsMitogen-Activated Protein Kinase 1Caspase 8Mitogen-Activated Protein Kinase 3MAP kinase kinase kinaseKinaseAkt/PKB signaling pathwayReverse Transcriptase Polymerase Chain ReactionMacrophage Colony-Stimulating FactorMacrophagesCell DifferentiationCell BiologyHematologyFlow CytometryCell biologyEnzyme ActivationPhosphorylationSignal transductionProto-Oncogene Proteins c-aktSignal TransductionBlood
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Pterostilbene Prevents Early Diabetic Retinopathy Alterations in a Rabbit Experimental Model

2019

Oxidative stress generated by diabetes plays a key role in the development of diabetic retinopathy (DR), a common diabetic complication. DR remains asymptomatic until it reaches advanced stages, which complicate its treatment. Although it is known that good metabolic control is essential for preventing DR, knowledge of the disease is incomplete and an effective treatment with no side effects is lacking. Pterostilbene (Pter), a natural stilbene with good antioxidant activity, has proved to beneficially affect different pathologies, including diabetes. Therefore, our study aimed to analyse the protective and/or therapeutic capacity of Pter against oxidant damage by characterising early retina…

Male0301 basic medicinepterostilbenePterostilbeneretinal damageNF-E2-Related Factor 2lcsh:TX341-641Pharmacologymedicine.disease_causeAntioxidantsArticlePhosphatidylinositol 3-Kinases03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDiabetes mellitusStilbenesmedicineAnimalsoxidative stressProtein kinase BPI3K/AKT/mTOR pathwayType 1 diabetesGlycogen Synthase Kinase 3 betaNutrition and Dieteticsbusiness.industryDiabetic retinopathymedicine.diseaseEnzyme ActivationDisease Models Animaldiabetic retinopathypolyphenol030104 developmental biologychemistryHyperglycemia030220 oncology & carcinogenesisMetabolic control analysisRabbitsbusinesslcsh:Nutrition. Foods and food supplyProto-Oncogene Proteins c-aktOxidative stressSignal TransductionFood ScienceNutrients
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Inhibition of Xanthine Oxidase by Allopurinol Prevents Skeletal Muscle Atrophy: Role of p38 MAPKinase and E3 Ubiquitin Ligases

2012

International audience; Abstract Top Alterations in muscle play an important role in common diseases and conditions. Reactive oxygen species (ROS) are generated during hindlimb unloading due, at least in part, to the activation of xanthine oxidase (XO). The major aim of this study was to determine the mechanism by which XO activation causes unloading-induced muscle atrophy in ratsand its possible prevention by allopurinol, a well-known inhibitor of this enzyme. For this purpose we studied one of the main redox sensitive signalling cascades involved in skeletal muscle atrophy i.e. p38 MAPKinaseand the expression of two well known muscle specific E3 ubiquitin ligases involved in proteolysis, …

MaleAgingAnatomy and Physiology[SDV]Life Sciences [q-bio]lcsh:MedicineMuscle ProteinsGene ExpressionHindlimbSignal transductionmedicine.disease_causep38 Mitogen-Activated Protein KinasesTripartite Motif Proteinschemistry.chemical_compound0302 clinical medicineMolecular cell biologySignaling in Cellular Processeslcsh:ScienceMusculoskeletal System0303 health sciencesMultidisciplinarySignaling cascadesMuscle BiochemistryAnimal ModelsMuscle atrophy3. Good healthMuscular Atrophymedicine.anatomical_structureBiochemistryHindlimb SuspensionMuscleMedicinemedicine.symptomCellular Typesmedicine.drugResearch Articlemedicine.medical_specialtyXanthine OxidaseMAPK signaling cascadesAllopurinolUbiquitin-Protein LigasesAllopurinolBiology03 medical and health sciencesAtrophyModel OrganismsInternal medicinemedicineAnimalsRats WistarXanthine oxidaseMuscle SkeletalBiology030304 developmental biologySoleus muscleMuscle CellsSKP Cullin F-Box Protein LigasesSuperoxide Dismutaselcsh:RSkeletal musclemedicine.diseaseRatsEnzyme ActivationOxidative StressEndocrinologychemistryRatlcsh:QPhysiological Processes030217 neurology & neurosurgeryOxidative stress
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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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Xenobiotic metabolizing enzymes of rat liver nonparenchymal cells.

1986

Abstract The nonparenchymal cells (NPC) of the liver are primarily located along the sinusoids and therefore are the first cells to encounter blood-borne xenobiotics. To study the possible role of the NPC in the metabolism of xenobiotics, populations of NPC and parenchymal cells (PC) were prepared from rats and various xenobiotic metabolizing enzyme activities investigated. The specific activity of every enzyme studied (ethoxyresorufin deethylase, benzphetamine demethylase, glutathione transferase, UDP glucuronosyltransferase, and microsomal epoxide hydrolase) was 12 to 1000% higher in the PC than in the NPC populations and the patterns of activities between the two populations were remarka…

MaleAroclorsCell SurvivalCellBiologyToxicologychemistry.chemical_compoundotorhinolaryngologic diseasesmedicineAnimalsCytotoxicityPharmacologychemistry.chemical_classificationL-Lactate DehydrogenaseRats Inbred StrainsMetabolismDNAChlorodiphenyl (54% Chlorine)Polychlorinated BiphenylsRatsEnzyme Activationstomatognathic diseasesEnzymemedicine.anatomical_structurechemistryBiochemistryLiverMicrosomal epoxide hydrolaseToxicitySpecific activityXenobioticToxicology and applied pharmacology
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The associated expression of Maspin and Bax proteins as a potential prognostic factor in intrahepatic cholangiocarcinoma

2006

Abstract Background Maspin, a member of the serpin family, is a suppressor of tumor growth, an inhibitor of angiogenesis and an inducer of apoptosis. Maspin induces apoptosis by increasing Bax, a member of the Bcl-2 family of apoptosis-regulating proteins. In this exploratory study, we investigated the associated expression of Maspin and Bax proteins as a potential prognostic factor in intrahepatic cholangiocarcinoma (IHCCA). Methods Twenty-two paraffin-embedded samples were analyzed by immunohistochemical methods using Maspin, Bax and CD34 antibodies. Maspin was scored semiquantitatively (HSCORE). Apoptosis was assessed using an antibody against cleaved caspase-3. Results The strong relati…

MaleCancer ResearchPathologymedicine.medical_specialtyAngiogenesisApoptosisCaspase 3Kaplan-Meier EstimateSerpinlcsh:RC254-282law.inventionCholangiocarcinomaBcl-2-associated X proteinlawBiomarkers TumorGeneticsmedicineHumansGenes Tumor SuppressorSerpinsIntrahepatic CholangiocarcinomaAgedbcl-2-Associated X ProteinbiologyCaspase 3business.industryMicrocirculationLiver NeoplasmsMaspinMiddle AgedPrognosislcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensNeoplasm ProteinsEnzyme ActivationOncologyApoptosisCancer researchbiology.proteinSuppressorFemalebusinessResearch ArticleBMC Cancer
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