Search results for "Mitogen-Activated Protein Kinase"

showing 10 items of 353 documents

Hepatoprotective and anti-inflammatory effects of total flavonoids of Qu Zhi Ke (peel of Citrus changshan-huyou) on non-alcoholic fatty liver disease…

2019

Abstract Background Citrus flavonoids, consisting of naringin, narirutin, neohesperidine, etc., have therapeutic activities for the treatment of lipometabolic disorders. The peel of Citrus changshan-huyou (Qu Zhi Ke, QZK) is a new source of flavonoids, but attracted little attention so far. Hypothesis QZK should possess therapeutic effects against lipometabolic disorders due to the flavonoids it contains. Study design In this study, we extracted and purified the flavonoids of QZK (TFCH) and established an obesity-induced non-alcoholic fatty liver disease (NAFLD) model of rats. TFCH was given orally for 8 weeks, and its anti-NAFLD effects and potential mechanism were evaluated. Methods The f…

MaleCitrusmedicine.drug_classFlavonoidPharmaceutical SciencePharmacologyDiet High-FatProtective AgentsAnti-inflammatoryProinflammatory cytokineRats Sprague-Dawley03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotNon-alcoholic Fatty Liver DiseaseDrug DiscoveryNonalcoholic fatty liver diseasemedicineAnimalsPhosphorylationNaringin030304 developmental biologyFlavonoidsPharmacologychemistry.chemical_classification0303 health sciencesNarirutinmedicine.diagnostic_testPlant ExtractsAnti-Inflammatory Agents Non-SteroidalFatty liverNF-kappa Bfood and beveragesmedicine.diseaseGene Expression RegulationLiverComplementary and alternative medicinechemistry030220 oncology & carcinogenesisMolecular MedicineMitogen-Activated Protein KinasesPhytomedicine
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Transcriptional profiling reveals functional links between RasGrf1 and Pttg1 in pancreatic beta cells

2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License .

MaleComputingMilieux_LEGALASPECTSOFCOMPUTINGTranscriptomeCytosolRas-GRF1Insulin-Secreting CellsGlucose homeostasisPromoter Regions GeneticOligonucleotide Array Sequence AnalysisMice KnockoutGeneticsCell biologySecurinERKPhenotypemedicine.anatomical_structureMitogen-Activated Protein KinasesBeta cellSignal transductionResearch ArticleSignal TransductionBiotechnologyCell signalingMedicina InvestigacióMedicinaPancreatic isletsBiologyGeneticsmedicineAnimalsCell LineagePttg1TranscriptomicsTranscription factorBinding Sitesras-GRF1Gene Expression ProfilingPancreatic isletsBeta cellsMolecular Sequence AnnotationGlucose Tolerance TestMice Inbred C57BLPàncrees MalaltiesGenetic LociData_GENERALTranscriptional factorsras ProteinsCalciumRasGrf1RasBMC Genomics
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Studies on protein kinases involved in regulation of nucleocytoplasmic mRNA transport

1988

The rate of energy-dependent nucleoside triphosphatase (NTPase)-mediated nucleocytoplasmic translocation of poly(A)-containing mRNA [poly(A)+mRNA] across the nuclear envelope is thought to be regulated by poly(A)-sensitive phosphorylation and dephosphorylation of nuclear-envelope protein. Studying the phosphorylation-related inhibition of the NTPase, we found that phosphorylation of one polypeptide of rat liver envelopes by endogenous NI- and NII-like protein kinase was particularly sensitive to poly(A). This polypeptide (106 kDa) was also phosphorylated by nuclear-envelope-bound Ca2+-activated and phospholipid-dependent protein kinase (protein kinase C). Activation of kinase C by tumour-pr…

MaleCytoplasmNuclear EnvelopeMitogen-activated protein kinase kinasePhosphatidylinositolsBiochemistryMAP2K7AnimalsRNA Messengerc-RafProtein kinase AMolecular BiologyProtein Kinase CProtein kinase CCell NucleusMembrane GlycoproteinsMAP kinase kinase kinasebiologyCyclin-dependent kinase 2Membrane ProteinsNuclear ProteinsBiological TransportRats Inbred StrainsCell BiologyMolecular biologyRatsNuclear Pore Complex ProteinsMicroscopy ElectronLiverBiochemistrybiology.proteinCyclin-dependent kinase 9PeptidesPoly AResearch ArticleBiochemical Journal
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Negative regulation of diacylglycerol kinase θ mediates adenosine-dependent hepatocyte preconditioning

2010

In liver ischemic preconditioning (IP), stimulation of adenosine A2a receptors (A2aR) prevents ischemia/reperfusion injury by promoting diacylglycerol-mediated activation of protein kinase C (PKC). By concerting diacylglycerol to phosphatidic acid, diacylglycerol kinases (DGKs) act as terminator of diacylglycerol signalling. This study investigates the role of DGK in the development of hepatocyte IP. DGK activity and cell viability were evaluated in isolated rat hepatocytes preconditioned by 10 min hypoxia followed by 10 min re-oxygenation or by the treatment with the A2aR agonist, CGS21680, and subsequently exposed to prolonged hypoxia. We observed that after IP or A2aR activation, a decre…

MaleDiacylglycerol Kinasemedicine.medical_specialtyAdenosineReceptor Adenosine A2Ap38 mitogen-activated protein kinasesBiologyQuinazolinonechemistry.chemical_compoundPiperidinecytoprotectionPiperidinesDownregulation and upregulationDiacylglycerol kinase thetaInternal medicinemedicineEnzyme Inhibitorhepatocytes adenosine RhoA hypoxia cytoprotectionAnimalsHepatocyteEnzyme InhibitorsRats WistarMolecular BiologyCells CulturedProtein kinase CQuinazolinonesDiacylglycerol kinaseCell DeathAnimalhypoxiaKinaseReceptors Purinergic P1RhoACell BiologyPhosphatidic acidAdenosineCell HypoxiaRatsCell biologyEndocrinologychemistryHepatocytesRatrhoA GTP-Binding Proteinmedicine.drugCell Death & Differentiation
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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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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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Genome-wide association and longitudinal analyses reveal genetic loci linking pubertal height growth, pubertal timing and childhood adiposity

2013

The pubertal height growth spurt is a distinctive feature of childhood growth reflecting both the central onset of puberty and local growth factors. Although little is known about the underlying genetics, growth variability during puberty correlates with adult risks for hormone-dependent cancer and adverse cardiometabolic health. The only gene so far associated with pubertal height growth, LIN28B, pleiotropically influences childhood growth, puberty and cancer progression, pointing to shared underlying mechanisms. To discover genetic loci influencing pubertal height and growth and to place them in context of overall growth and maturation, we performed genome-wide association meta-analyses i…

MaleNetherlands Twin Register (NTR)Genetic LinkageMedizinGene ExpressionGenome-wide association studyVARIANTSBody Mass Index0302 clinical medicinegenetic linkageTransforming Growth Factor betaNeoplasmsmolecular biologygeneticsChildGenetics (clinical)Adiposity2. Zero hunger0303 health sciencesadiposityMitogen-Activated Protein Kinase 3Association Studies ArticlesAge FactorsACHONDROPLASIAGeneral MedicineGenome-Wide Association Study; pubertal height growth; pubertal timingPhenotypeOBESITYMenarche/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingbody heightFemaleSignal Transductionmedicine.medical_specialtyage factorsCHROMOSOME 16P11.2AdolescentBIRTHQuantitative Trait Loci030209 endocrinology & metabolismContext (language use)BiologyChildhood obesitypubertal height growthMENARCHEYoung Adult03 medical and health sciencesAGESDG 3 - Good Health and Well-beingPrepubertyInternal medicineGeneticsmedicine/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_HumansMolecular Biology030304 developmental biologySignMenarcheFACTOR RECEPTOR-3MUTATIONSpubertal timingPubertyta3121medicine.diseaseObesityBody HeightGenetic architectureEndocrinologyPOPULATION COHORTgene expressionBody mass indexFollow-Up StudiesGenome-Wide Association Study
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