Search results for "Mitogen-Activated Protein Kinase"

showing 10 items of 353 documents

Nonsense-mediated mRNA decay controls the changes in yeast ribosomal protein pre-mRNAs levels upon osmotic stress.

2013

The expression of ribosomal protein (RP) genes requires a substantial part of cellular transcription, processing and translation resources. Thus, the RP expression must be tightly regulated in response to conditions that compromise cell survival. In Saccharomyces cerevisiae cells, regulation of the RP gene expression at the transcriptional, mature mRNA stability and translational levels during the response to osmotic stress has been reported. Reprogramming global protein synthesis upon osmotic shock includes the movement of ribosomes from RP transcripts to stress-induced mRNAs. Using tiling arrays, we show that osmotic stress yields a drop in the levels of RP pre-mRNAs in S. cerevisiae cell…

OsmosisTranscription GeneticNonsense-mediated decaylcsh:MedicineYeast and Fungal ModelsMolecular cell biologyGene Expression Regulation FungalGene expressionProtein biosynthesisRNA PrecursorsRNA Processing Post-Transcriptionallcsh:ScienceOligonucleotide Array Sequence AnalysisCellular Stress ResponsesRegulation of gene expressionMultidisciplinarybiologyProtein translationExonsGenomicsCell biologyFunctional GenomicsMitogen-activated protein kinaseResearch ArticleRibosomal ProteinsSaccharomyces cerevisiae ProteinsOsmotic shockEstrès oxidatiuSaccharomyces cerevisiaeGenes FungalDNA transcriptionSaccharomyces cerevisiaeModels BiologicalGenètica molecularSaccharomycesModel OrganismsRibosomal proteinStress PhysiologicalBiologylcsh:RRNA stabilitybiology.organism_classificationMolecular biologyIntronsNonsense Mediated mRNA DecayKineticsRNA processingbiology.proteinlcsh:QGene expressionGenome Expression AnalysisProteïnesPloS one
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Phospho-p38 MAPK expression in COPD patients and asthmatics and in challenged bronchial epithelium

2015

<b><i>Background:</i></b> The role of mitogen-activated protein kinases (MAPK) in regulating the inflammatory response in the airways of patients with chronic obstructive pulmonary disease (COPD) and asthmatic patients is unclear. <b><i>Objectives:</i></b> To investigate the expression of activated MAPK in lungs of COPD patients and in bronchial biopsies of asthmatic patients and to study MAPK expression in bronchial epithelial cells in response to oxidative and inflammatory stimuli. <b><i>Methods:</i></b> Immunohistochemical expression of phospho (p)-p38 MAPK, p-JNK1 and p-ERK1/2 was measured in bronchial mucosa in pat…

P38 MAPKMaleMAPK/ERK pathwayAsthma phenotypeSMOKERespiratory SystemMitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Chronic obstructive pulmonary disease phenotypes; Asthma phenotypesPathology of chronic obstructive pulmonary diseasep38 Mitogen-Activated Protein KinasesChronic obstructive pulmonary disease phenotypePulmonary Disease Chronic ObstructiveOXIDATIVE STRESSMACROPHAGESRespiratory systemMitogen-activated protein kinasesChronic obstructive pulmonary disease phenotypesMitogen-activated protein kinases; p65; pathology of chronic obstructive pulmonary disease phenotypes; asthma phenotypesCOPDp65KinaseAsthma phenotypes; Chronic obstructive pulmonary disease phenotypes; Mitogen-activated protein kinases; p65; Pathology of chronic obstructive pulmonary disease; Pulmonary and Respiratory MedicineACTIVATED PROTEIN-KINASEInterleukinMiddle AgedImmunohistochemistrypathology of chronic obstructive pulmonary disease phenotypesAsthma phenotypesFemaleLife Sciences & BiomedicinePulmonary and Respiratory Medicinep38 mitogen-activated protein kinasesBlotting WesternINHIBITIONSocio-culturaleBronchiRespiratory MucosaOBSTRUCTIVE PULMONARY-DISEASE1102 Cardiovascular Medicine And HaematologyCell LinemedicineHumansLymphocyte CountInterleukin 8AgedAsthmaScience & Technologybusiness.industryInterleukin-8Transcription Factor RelAPATHWAYSMitogen-activated protein kinasemedicine.diseaseAsthmarespiratory tract diseasesSEVERITYCase-Control StudiesCELLSImmunologybusiness
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Traditional Chinese herbal medicine at the forefront battle against COVID-19: Clinical experience and scientific basis.

2020

Abstract Background Throughout the 5000-year history of China, more than 300 epidemics were recorded. Traditional Chinese herbal medicine (TCM) has been used effectively to combat each of these epidemics’ infections, and saved many lives. To date, there are hundreds of herbal TCM formulae developed for the purpose of prevention and treatment during epidemic infections. When COVID-19 ravaged the Wuhan district in China in early January 2020, without a deep understanding about the nature of COVID-19, patients admitted to the TCM Hospital in Wuhan were immediately treated with TCM and reported later with >90% efficacy. Approach We conducted conduct a systematic survey of various TCM herbal pre…

PTGS2 Prostaglandin-endoperoxide synthase 2BattleAIV avian influenza virusCoV coronavirusPharmaceutical ScienceiNOS nitric oxide synthaseViral infection0302 clinical medicinePA patchouli alcoholSARS Severe Acute Respiratory SyndromeSMD Sheganmahuang decoctionDrug DiscoveryPandemicIL InterleukinMedicine Chinese TraditionalALI acute lung injuriesmedia_commonCOVID-19 coronavirus disease 2019MXSG Ma xing shi gan decoction0303 health sciencesTNF tumor necrosis factorClinical Trials as TopicCCL2 CC chemokine ligand 2FM1 FM1 coronavirusICU intensive care unitc-AMP cyclic adenosine phosphateHIV human immunodeficiency virus030220 oncology & carcinogenesisCOX-2 cyclooxygenase-2Molecular MedicineHerbal preparationsMedicinal herbsAbbreviations: ACE2 angiotensin-converting enzyme IITCM traditional Chinese medicineHSV-1 herpes simplex virus 1CASP3 caspase 3medicine.medical_specialtyChinaCoronavirus disease 2019 (COVID-19)Systematic surveymedia_common.quotation_subjectJEV Japanese encephalitis virusNF-κB nuclear factor kappa B cellsAntiviral AgentsArticleWHO World Health Organization03 medical and health sciencesIEC-6 rat intestinal epithelial cell line 6SOD superoxide dismutaseCDC Center for Disease Control and PreventionmedicineAVP arginine vasopressinPGE2 prostaglandin E2HumansIntensive care medicineLH Lianhuaqingwen capsule030304 developmental biologyPharmacologyMedicinal herbMDA malondialdehydeGCGJ Gancao ganjiang decoctionNO nitric oxidePlants Medicinalbusiness.industrySARS-CoV-2COVID-19CXCL C-X-C- motif chemokineMDCK Madin-Darby Canine Kidney cellsTLR-4 Toll-like receptor-4COVID-19 Drug TreatmentComplementary and alternative medicineViral infectionLPS lipopolysaccharidesRSV respiratory syncytial virusQFPD Qingfeipaidu decoctionbusinessLung congestionECMO extracorporeal membrane oxygenationMAPK mitogen-activated protein kinasePhytotherapyDrugs Chinese HerbalPhytomedicine : international journal of phytotherapy and phytopharmacology
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Effects of polyphenols and lipids from Pennisetum glaucum grains on T-cell activation: modulation of Ca2+ and ERK1/ERK2 signaling

2015

International audience; BACKGROUND: Pearl millet (PM), i.e., Pennisetum glaucum, is widely grown in Africa and known for its anti-oxidant and anti-hyperlipidemic properties.METHODS: The P. glaucum grains were obtained from the region of Ouled Aïssa (South of Algeria). We assessed the effects of phenolic compounds and lipids, extracted from seeds of P. glaucum, on rat lymphocyte proliferation, activated by phorbol 12-myristate 13-acetate and ionomycin. In order to explore signaling pathway, triggered by these compounds, we assessed interleukin-2 (IL-2) mRNA expression and extracellular signal-regulated kinase-1/2 (ERK1/ERK2) phosphorylation. Finally, we determined increases in free intracell…

PennisetumT-LymphocytesLymphocyte proliferationLymphocyte ActivationAntioxidantsPearl milletchemistry.chemical_compoundExtracellularAnimalsGallic acidExtracellular Signal-Regulated MAP KinasesCell ProliferationHypolipidemic AgentsMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologybiologyPlant ExtractsT-cellsPolyphenolsGeneral Medicinebiology.organism_classificationLipidsRatschemistryBiochemistryComplementary and alternative medicinePolyphenolIonomycinSeedsPhorbolPhosphorylationCalciumEdible GrainPennisetum[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologySignal TransductionResearch Article
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Shikonin reduces oedema induced by phorbol ester by interfering with IκBα degradation thus inhibiting translocation of NF-κB to the nucleus

2010

Background and purpose In the present paper we studied the effect of shikonin on ear oedema induced by 12-O-tetradecanoylphorbol-13-acetate (TPA), and determined the mechanisms through which shikonin might exert its topical anti-inflammatory action. Experimental approach Acute ear oedema was induced in mice by topical application of TPA. The in vitro assays used macrophages RAW 264.7 cells stimulated with lipopolysaccharide. Cyclooxygenase-2, inducible nitric oxide synthase, protein kinase Calpha, extracellular signal-regulated protein kinase (ERK), phosphorylated ERK (pERK), c-Jun N-terminal kinase (JNK), pJNK, p38, p-p38, p65, p-p65, inhibitor protein of nuclear factor-kappaB (NF-kappaB) …

PharmacologyMAPK/ERK pathwayIκBαKinasep38 mitogen-activated protein kinasesMitogen-activated protein kinasebiology.proteinElectrophoretic mobility shift assayBiologyNFKB1Protein kinase AMolecular biologyBritish Journal of Pharmacology
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The carbon monoxide-releasing molecule CORM-2 inhibits the inflammatory response induced by cytokines in Caco-2 cells

2007

Background and purpose: Recent evidence indicates that carbon monoxide-releasing molecules (CO-RMs) exhibit potential anti-inflammatory properties. In the present study, we have investigated whether tricarbonyl dichloro ruthenium(II) dimer (CORM-2) can control the inflammatory response induced by cytokines in a human colonic epithelial cell line, Caco-2. Experimental approach: Caco-2 cells were preincubated with CORM-2 for 30 minutes and then stimulated with interleukin (IL)-1β, tumor necrosis factor-α and interferon-γ for different times. Gene expression was analyzed by real-time PCR. Protein expression was investigated by Western blot and ELISA. Transcription factor activation was determi…

PharmacologySmall interfering RNACytokinep38 mitogen-activated protein kinasesEnhancer bindingmedicine.medical_treatmentGene expressionmedicineTumor necrosis factor alphaBiologyNFKB1Protein kinase AMolecular biologyBritish Journal of Pharmacology
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Involvement of protein kinases in the induction of NO synthase II in human DLD-1 cells

1998

Protein phosphorylation is involved in the induction of nitric oxide synthase II (NOS II, iNOS) in several types of animal cells. Here we have investigated the possible involvement of major protein kinases in the induction of NOS II expression in human DLD-1 cells. In DLD-1 cells, interferon-γ alone induced a submaximal NOS II expression; a cytokine mixture consisting of interferon-γ, tumour necrosis factor-α and interleukin-1β produced maximal NOS II induction. Activators of protein kinase A (forskolin, 8-dibutyryl-cyclic AMP), of protein kinase C (tetradecanoylphorbol-13-acetate), and of protein kinase G (8-bromo cyclic GMP) did not induce NOS II mRNA by themselves, nor did they alter NOS…

PharmacologybiologyMAP kinase kinase kinaseCyclin-dependent kinase 4Cyclin-dependent kinase 2biology.proteinCyclin-dependent kinase 9ASK1c-RafMitogen-activated protein kinase kinaseMolecular biologyMAP2K7British Journal of Pharmacology
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n-3 PUFAs modulate T-cell activation via protein kinase C-α and -ε and the NF-κB signaling pathway

2005

We elucidated the mechanisms of action of two n-3 PUFAs, eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), in Jurkat T-cells. Both DHA and EPA were principally incorporated into phospholipids in the following order: phosphatidylcholine < phosphatidylethanolamine < phosphatidylinositol/phosphatidylserine. Furthermore, two isoforms of phospholipase A(2) (i.e., calcium-dependent and calcium-independent) were implicated in the release of DHA and EPA, respectively, during activation of these cells. The two fatty acids inhibited the phorbol 12-myristate 13-acetate (PMA)-induced plasma membrane translocation of protein kinase C (PKC)-alpha and -epsilon. The two n-3 PUFAs also inhibited t…

PhosphatidylethanolaminePhospholipase Amitogen-activated protein kinaseProtein Kinase C-epsilonQD415-436Cell BiologyPhosphatidylserineBiologyfatty acidsBiochemistryJurkat cellsCell biologychemistry.chemical_compoundEndocrinologychemistryBiochemistryDocosahexaenoic acidlipids (amino acids peptides and proteins)Phosphatidylinositolnuclear factor κBProtein kinase Cpolyunsaturated fatty acidsJournal of Lipid Research
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Pore-forming toxins activate MAPK p38 by causing loss of cellular potassium.

2009

Mitogen activated protein kinase (MAPK) p38 has emerged as a survival protein in cells that are attacked by bacterial toxins forming small membrane pores. Activation of p38 by pore forming toxins (PFT) has been attributed to osmotic stress, but here we show that loss of K+ is likely to be the critical parameter. Several lines of evidence support this conclusion: first, osmoprotection did not prevent p38-phosphorylation in alpha-toxin-loaded cells. Second, treatment of cells with a K+ ionophore, or simple incubation in K+-free medium sufficed to cause robust p38-phosphorylation. Third, media containing high [K+] prevented p38-activation by Staphylococcus aureus alpha-toxin, Vibrio cholerae c…

Pore Forming Cytotoxic ProteinsOsmotic shockp38 mitogen-activated protein kinasesBacterial ToxinsBiophysicsBiologyHemolysin ProteinsBiochemistryp38 Mitogen-Activated Protein KinasesCell LineCell membraneHemolysin ProteinsmedicineHumansPhosphorylationMolecular BiologyPore-forming toxinEscherichia coli ProteinsCell MembraneHemolysinEpithelial CellsCell BiologyCell biologyEnzyme Activationmedicine.anatomical_structureBiochemistryPotassiumStreptolysinCalciumCytolysinBiochemical and biophysical research communications
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Antitumor effects of dehydroxymethylepoxyquinomicin, a novel nuclear factor-kappaB inhibitor, in human liver cancer cells are mediated through a reac…

2009

Activation of the nuclear transcription factor-kappa B (NF-kappa B) has been implicated in liver tumorigenesis. We evaluated the effects of a novel NF-kappa B inhibitor, dehydroxymethylepoxyquinomicin (DHMEQ), in two human liver cancer cell lines HA22T/VGH and HuH-6. DHMEQ treatment dose dependently decreased the DNA-binding capacity of the NF-kappa B p65 subunit, inhibited cell growth and proliferation, and increased apoptosis as shown by caspase activation, release of cytochrome c, poly(ADP-ribose) polymerase cleavage, and down-regulation of survivin. DHMEQ also induced a dose-dependent activation of mitogen-activated protein kinase kinase/extracellular signal-regulated kinase signaling, …

Programmed cell deathCarcinoma HepatocellularBIOLOGICAL-ACTIVITIESDrug Evaluation PreclinicalDown-RegulationAntineoplastic AgentsApoptosisBiologymedicine.disease_causeACTIVATIONchemistry.chemical_compoundHYDROGEN-PEROXIDEENDOPLASMIC-RETICULUM STRESSCell Line TumorSurvivinNADPH OXIDASEmedicineHumansOXIDATIVE STRESSProtein kinase AEndoplasmic Reticulum Chaperone BiPINDUCED APOPTOSISCell ProliferationPharmacologySettore MED/12 - GastroenterologiaDose-Response Relationship DrugUNFOLDED PROTEIN RESPONSECell growthCyclohexanonesINDUCTIONLiver NeoplasmsDEATHNF-kappa BCytochromes cMolecular biologyCell biologyEnzyme ActivationchemistryApoptosisCaspasesCancer cellBenzamidesSettore BIO/14 - FarmacologiaMolecular MedicineGrowth inhibitionMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesReactive Oxygen SpeciesOxidative stressMolecular pharmacology
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