Search results for "Mapk"

showing 10 items of 238 documents

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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SARS CoV2 infection _The longevity study perspectives

2021

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MaleAgingssRNA single-stranded RNARFLP restriction fragment length polymorphismHSPs heat shock proteinsReviewPTMs post-translational modificationsSevere Acute Respiratory SyndromeBiochemistryHIV-1 human immunodeficiency virus-1TNF-α tumor necrosis factor-αEC endothelial cells0302 clinical medicineFluAV influenza A virusI insertionMedicineIFN-γ interferon-γDIC disseminated intravascular coagulationPCR Polymerase Chain Reactionmedia_commonAged 80 and overLongevityRBD receptor-binding domainNeurologyLongevity modelMI myocardial infarctionNK natural killerhPIV2 human parainfluenza virus type 2media_common.quotation_subjectResearching genetic basis of resistance and potential pharmacological targetsLongevityDBP diastolic blood pressureNF-Kb nuclear transcription factor kBRANTES regulated upon activation normal T cell expressed and secretedMphi human macrophages03 medical and health sciencesCox 2 cyclooxygenase 2ORF open reading framePT prothrombin timeSettore MED/05 - Patologia ClinicaHumansMolecular BiologyInflammatory genesARDS acute respiratory distress syndromeNO nitric oxideD deletionCpGIs CpG islandsT2DM type 2 diabetes mellitusmedicine.diseaseFDP fibrin degradation products030104 developmental biologySARS CoV2 severe acute respiratory syndrome Coronavirus 2 virusImmunologyBMI body max indexItalian nonagenarians/centenariansRSV respiratory syncytial virusComplication030217 neurology & neurosurgeryMAPK mitogen-activated protein kinaseIP-10 IFN-γ -Inducible Protein 1040301 basic medicineAT1R activity of angiotensin 1 receptorsDCs dentritic cellsSSCP single strand conformation polymorphismACE/DD polymorphism of the angiotensin converting enzymeFGF21 fibroblast growth factor 21TLR4 toll-like receptor 4NAD nicotinamide adenine dinucleotideACE angiotensin-I converting enzymeAT2R activity of angiotensin 2 receptorsCOVID-19 Coronavirus disease 2019Respiratory distressACE2 angiotensin converting enzyme 2MKP-1 mitogen-activated protein kinase phosphatase-1 ()PD protease domainSNP single nucleotide polymorphismEH essential hypertensionTNFR tumor necrosis factor receptorINR international normalized ratio of the prothrombin timePAI-1 plasminogen activator inhibitor-1Ang angiotensinLPS lipopolysaccharideMCP1 monocyte chemoattractant protein-1medicine.symptomaPTT partial thromboplastin timeBiotechnologyDUSP1 dual specificity phosphatase 1Coronavirus disease 2019 (COVID-19)PC prostate cancerRAS renin-angiotensin aldosterone systemCCR5Δ32 genetic variant of chemokine receptorCOVID-19 Researching genetic basis of resistance and potential pharmacological targets Italian nonagenarians/centenarians Longevity modelAsymptomaticSARS-1 severe acute respiratory syndrome virus 1SIRT-1 Sirtuin 1Th1 t-helper lymphocyte type 1Immune systemROS reactive oxygen speciesTGF-β transforming growth factor betaET-1 endothelin-1ComputingMethodologies_COMPUTERGRAPHICSADAM-17 metallopeptidase domain 17business.industrySARS-CoV-2SBP systolic blood pressureCOVID-19HDACs histone deacetylasesComorbidityImmune Systembusiness5-LO lipoxygenase 5Ageing Research Reviews
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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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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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Females Live Longer than Males: Role of Oxidative Stress

2011

One of the most significant achievements of the twentieth century is the increase in human lifespan. In any period studied, females live longer than males. We showed that mitochondrial oxidative stress is higher in males than females and that the higher levels of estrogens in females protect them against ageing, by up-regulating the expression of antioxidant, longevity-related genes. The chemical structure of estradiol confers antioxidant properties to the molecule. However, the low concentration of estrogens in females makes it unlikely that they exhibit significant antioxidant capacity in the organism. Therefore we studied the mechanisms enabling estradiol to be antioxidant at physiologic…

MaleMAPK/ERK pathwayAgingmedicine.medical_specialtyAntioxidantCell Survivalmedicine.medical_treatmentEstrogen receptorGenisteinPhytoestrogensBiologymedicine.disease_causeAntioxidantschemistry.chemical_compoundLife ExpectancyCell Line TumorInternal medicineDrug DiscoverymedicineAnimalsHumansReceptorPharmacologySex CharacteristicsMolecular StructureEstrogensMitochondriaOxidative StressEndocrinologyReceptors EstrogenchemistryAgeingFemalePhytoestrogensReactive Oxygen Specieshormones hormone substitutes and hormone antagonistsOxidative stressProtein BindingCurrent Pharmaceutical Design
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Dephosphorylation of p-ERK1/2 in relation to tumor remission after HER-2 and Raf1 blocking therapy in a conditional mouse tumor model

2006

Several studies have shown that HER-2/neu (erbB-2) blocking therapy strategies can cause tumor remission. However, the responsible molecular mechanisms are not yet known. Both ERK1/2 and Akt/PKB are critical for HER-2-mediated signal transduction. Therefore, we used a mouse tumor model that allows downregulation of HER-2 in tumor tissue by administration of anhydrotetracycline (ATc). Switching-off HER-2 caused a rapid tumor remission by more than 95% within 7 d of ATc administration compared to the volume before switching-off HER-2. Interestingly, HER-2 downregulation caused a dephosphorylation of p-ERK1/2 by more than 80% already before tumor remission occurred. Levels of total ERK protein…

MaleMAPK/ERK pathwayCancer Researchmedicine.medical_specialtyReceptor ErbB-2Blotting WesternDown-RegulationMice NudeP erk1 2BiologyTransfectionDephosphorylationMiceDownregulation and upregulationInternal medicinemedicineAnimalsHumansMouse tumorPhosphorylationMolecular BiologyProtein kinase BMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Remission InductionNeoplasms ExperimentalTumor tissueGene Expression Regulation NeoplasticProto-Oncogene Proteins c-rafDisease Models AnimalEndocrinologyTetracyclinesNIH 3T3 CellsCancer researchSignal transductionSignal TransductionMolecular Carcinogenesis
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Pentoxifylline Prevents Loss of PP2A Phosphatase Activity and Recruitment of Histone Acetyltransferases to Proinflammatory Genes in Acute Pancreatitis

2009

Mitogen-activated protein kinases (MAPKs) are considered major signal transducers early during the development of acute pancreatitis. Pentoxifylline is a phosphodiesterase inhibitor with marked anti-inflammatory properties through blockade of extracellular signal regulated kinase (ERK) phosphorylation and tumor necrosis factor alpha production. Our aim was to elucidate the mechanism of action of pentoxifylline as an anti-inflammatory agent in acute pancreatitis. Necrotizing pancreatitis induced by taurocholate in rats and taurocholate-treated AR42J acinar cells were studied. Phosphorylation of ERK and ERK kinase (MEK1/2), as well as PP2A, PP2B, and PP2C serine/threonine phosphatase activiti…

MaleMAPK/ERK pathwayChromatin ImmunoprecipitationPhosphodiesterase InhibitorsBlotting WesternPhosphataseAnti-Inflammatory AgentsPharmacologyBiologyCell LinePentoxifyllineProinflammatory cytokineCyclic AMPPhosphoprotein PhosphatasesmedicineAnimalsPentoxifyllineRats WistarExtracellular Signal-Regulated MAP KinasesHistone AcetyltransferasesInflammationPharmacologyReverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaProtein phosphatase 2medicine.diseaseCyclic Nucleotide Phosphodiesterases Type 2RatsEnzyme ActivationPancreatitisBiochemistryAcute DiseaseRNAMolecular MedicinePhosphorylationPancreatitisMitogen-Activated Protein KinasesChromatin immunoprecipitationmedicine.drugJournal of Pharmacology and Experimental Therapeutics
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Phosphorylation of extracellular signal-related protein kinase is required for rapid facilitation of heat-induced currents in rat dorsal root ganglio…

2005

A subgroup of dorsal root ganglion (DRG) neurons responds to noxious heat with an influx of cations carried by specific ion channels such as the transient receptor potential channel of the vanilloid receptor type, subtype 1 (TRPV1). Application of capsaicin induces a reversible facilitation of these currents. This facilitation could be an interaction of two agonists at their common receptor or be caused by an influx of calcium ions into the cell. Calcium influx into the cell can activate protein kinases such as the extracellular signal-related protein kinase (ERK) pathway. This study explored the kinetics, calcium-dependency and intracellular signals following application of capsaicin and l…

MaleMAPK/ERK pathwayHot TemperaturePatch-Clamp TechniquesStatistics as TopicTRPV1BiologyMembrane PotentialsRats Sprague-Dawleychemistry.chemical_compoundBAPTAGanglia SpinalNitrilesButadienesAnimalsDrug InteractionsEnzyme InhibitorsPhosphorylationExtracellular Signal-Regulated MAP KinasesProtein kinase AProtein kinase CNeuronsAnalysis of VarianceDose-Response Relationship DrugGeneral NeuroscienceMEK inhibitorRatsCell biologychemistryBiochemistryCapsaicinMitogen-activated protein kinasebiology.proteinCalciumFemaleCapsaicinNeuroscience
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Inactivation of glycogen synthase kinase-3β protects against kainic acid-induced neurotoxicity in vivo

2004

Many neurodegenerative diseases involve oxidative stress and excitotoxic cell death. In an attempt to further elucidate the signal transduction pathways involved in the cell death/cell survival associated with excitotoxicity, we have used an in vivo model of excitotoxicity employing kainic acid (KA)-induced neurotoxicity. Here, we show that extracellular signal-related kinase (ERK) 2, but not ERK 1, is phosphorylated and thereby activated in the hippocampus and cerebellum of kainic acid-treated mice. Phosphorylation and hence inactivation of glycogen synthase kinase 3beta (GSK-3beta), a general survival factor, is often a downstream consequence of mitogen-activated protein kinase pathway ac…

MaleMAPK/ERK pathwayKainic acidProgrammed cell deathTime FactorsCell SurvivalBlotting WesternExcitotoxicityTetrazolium Saltsmacromolecular substancesBiologymedicine.disease_causeHippocampusGlycogen Synthase Kinase 3Micechemistry.chemical_compoundOrgan Culture TechniquesGSK-3CerebellumNitrilesButadienesSerinemedicineAnimalsEnzyme InhibitorsPhosphorylationProtein kinase AMolecular BiologyMitogen-Activated Protein Kinase 1Glycogen Synthase Kinase 3 betaKainic AcidBehavior AnimalCell DeathKinaseGeneral NeuroscienceImmunohistochemistryCell biologyEnzyme ActivationThiazolesBiochemistrychemistryTyrosineNeurotoxicity SyndromesNeurology (clinical)Signal transductionLithium ChlorideDevelopmental BiologyBrain Research
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Plasticity-related gene-1 inhibits lysophosphatidic acid-induced vascular smooth muscle cell migration and proliferation and prevents neointima forma…

2012

International audience; Plasticity-related gene-1 (PRG-1) protects neuronal cells from lysophosphatidic acid (LPA) effects. In vascular smooth muscle cells (VSMCs), LPA was shown to induce phenotypic modulation in vitro and vascular remodeling in vivo. Thus we explored the role of PRG-1 in modulating VSMC response to LPA. PCR, Western blot, and immunofluorescence experiments showed that PRG-1 is expressed in rat and human vascular media. PRG-1 expression was strongly inhibited in proliferating compared with quiescent VSMCs both in vitro and in vivo (medial vs. neointimal VSMCs), suggesting that PRG-1 expression is dependent on the cell phenotype. In vitro, adenovirus-mediated overexpression…

MaleMAPK/ERK pathwayNeointimaVascular smooth musclePhysiologyPhenotypic modulation[SDV]Life Sciences [q-bio]Genetic VectorsBiologyPlasticityMuscle Smooth VascularAdenoviridaechemistry.chemical_compoundCell MovementNeointimaLysophosphatidic acidAnimalsHumansRats WistarCells CulturedCell ProliferationCell BiologyLipid-phosphate phosphatasePhosphoric Monoester HydrolasesIn vitroRatsCell biologyGene Expression RegulationchemistryBiochemistryCalmodulin-Binding ProteinsLysophospholipidsAmerican Journal of Physiology-Cell Physiology
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