Search results for "Mitogen-activated protein kinases"

showing 10 items of 246 documents

Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
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Activation of c-Jun N-terminal kinase 1 by UV irradiation is inhibited by wortmannin without affecting c-iun expression.

1999

Activation of c-Jun N-terminal kinases (JNKs)/stress-activated protein kinases is an early response of cells upon exposure to DNA-damaging agents. JNK-mediated phosphorylation of c-Jun is currently understood to stimulate the transactivating potency of AP-1 (e.g., c-Jun/c-Fos; c-Jun/ATF-2), thereby increasing the expression of AP-1 target genes. Here we show that stimulation of JNK1 activity is not a general early response of cells exposed to genotoxic agents. Treatment of NIH 3T3 cells with UV light (UV-C) as well as with methyl methanesulfonate (MMS) caused activation of JNK1 and an increase in c-Jun protein and AP-1 binding activity, whereas antineoplastic drugs such as mafosfamide, mito…

Alkylating AgentsProto-Oncogene Proteins c-junUltraviolet RaysStimulationBiologyenvironment and public healthWortmanninTransactivationchemistry.chemical_compoundMiceAnimalsPhosphatidylinositolCollagenasesProtein kinase AMolecular BiologyCell Growth and DevelopmentMitogen-Activated Protein Kinase 1Kinasec-junJNK Mitogen-Activated Protein KinasesCell Biology3T3 CellsMethyl MethanesulfonateMolecular biologyAndrostadienesEnzyme ActivationGene Expression Regulation NeoplasticTranscription Factor AP-1chemistryCalcium-Calmodulin-Dependent Protein KinasesPhosphorylationMitogen-Activated Protein KinasesWortmanninMolecular and cellular biology
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Detection of mitochondrial electron chain carrier redox status by transhepatic light intensity during rat liver reperfusion.

2003

The aim of the study was to investigate mitochondrial electron transfer during rat liver reperfusion after cold storage and hypothermic machine perfusion. Livers from male Brown Norway rats were preserved (UW) for 10h either by cold storage (CS) or by hypothermic oxygenated perfusion extracorporal (HOPE). Transhepatic photometric analysis allowed determination of the redox status of mitochondrial cytochromes during preservation, rewarming and reperfusion. Mitochondrial electron chain carriers were inhibited at different sites with rotenone and cyanide in some experiments. reversed transcriptional polymerase chain reaction (RT-PCR) was performed after reperfusion concerning transcription of …

AnionsMaleTime FactorsCytochromeLightCold storageCaspase 3ElectronsDNA FragmentationMitochondrionGeneral Biochemistry Genetics and Molecular Biologychemistry.chemical_compoundSuperoxidesAnimalsCaspase-9CryopreservationCyanidesbiologySuperoxideCaspase 3Reverse Transcriptase Polymerase Chain ReactionTumor Necrosis Factor-alphaJNK Mitogen-Activated Protein KinasesTemperatureNADH DehydrogenaseGeneral MedicineRotenoneDNAOrgan PreservationLipid MetabolismCaspase 9MitochondriaRatsCold TemperatureOxygenLight intensitychemistryBiochemistryElectron Transport Chain Complex ProteinsLiverCaspasesReperfusionbiology.proteinCytochromesLipid PeroxidationMitogen-Activated Protein KinasesGeneral Agricultural and Biological SciencesReactive Oxygen SpeciesOxidation-ReductionCryobiology
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A role for the MAP kinase gene MKC1 in cell wall construction and morphological transitions in Candida albicans.

1998

The Candida albicans MKC1 gene encodes a mitogen-activated protein (MAP) kinase, which has been cloned by complementation of the lytic phenotype associated with Saccharomyces cerevisiae slt2 (mpk1) mutants. In this work, the physiological role of this MAP kinase in the pathogenic fungus C. albicans was characterized and a role for MKC1 in the biogenesis of the cell wall suggested based on the following criteria. First, C. albicans mkc1Δ/mkc1Δ strains displayed alterations in their cell surfaces under specific conditions as evidenced by scanning electron microscopy. Second, an increase in specific cell wall epitopes (O-glycosylated mannoprotein) was shown by confocal microscopy in mkc1Δ/mkc1…

Antifungal AgentsTranscription GeneticSaccharomyces cerevisiaeMutantMAP Kinase Kinase 2MAP Kinase Kinase 1ChitinSaccharomyces cerevisiaeProtein Serine-Threonine KinasesMicrobiologyGene Expression Regulation EnzymologicFungal ProteinsPseudohyphal growthCell WallGene Expression Regulation FungalCandida albicansCandida albicansDNA FungalFluorescent Antibody Technique IndirectGlucansProtein Kinase CMitogen-Activated Protein Kinase KinasesRecombination GeneticMembrane GlycoproteinsMicroscopy ConfocalbiologyKinaseProtein-Tyrosine Kinasesbiology.organism_classificationFlow Cytometrybeta-GalactosidaseCorpus albicansComplementationMicroscopy ElectronBiochemistryMitogen-activated protein kinaseCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinMicroscopy Electron ScanningMitogen-Activated Protein KinasesPlasmidsMicrobiology (Reading, England)
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Thiol antioxidants block the activation of antigen-presenting cells by contact sensitizers.

2003

Strong contact sensitizers are able to induce signal transduction mechanisms such as tyrosine phosphorylation and activation of MAP kinases in antigen-presenting cells. We studied the capacity of different antioxidants (ascorbic acid, alpha-tocopherol, pyrrolidine dithiocarbamate, N-acetylcysteine, and glutathione) to block the increase in tyrosine phosphorylation in human monocytes seen after stimulation with strong contact sensitizers. Human peripheral blood mononuclear cells were stimulated with 5-chloro-2-methylisothiazolinone plus 2-methylisothiazolinone in the presence or absence of these antioxidants. The total amount of membrane-associated phosphotyrosine in CD14+ cells was quantifi…

Antigen-Presenting CellsDermatologyPicryl ChlorideDermatitis ContactBiochemistryAntioxidantschemistry.chemical_compoundPyrrolidine dithiocarbamateHumansdendritic cellsCysteineSulfhydryl CompoundsTyrosinePhosphorylationAntigen-presenting cellMolecular BiologyCells CulturedNF-kappa BTyrosine phosphorylationCell BiologyGlutathioneAscorbic acidGlutathioneAcetylcysteineMAP kinaseschemistryBiochemistrycontact sensitizerthiol antioxidantTyrosineSignal transductionMitogen-Activated Protein KinasesmonocytesCysteineThe Journal of investigative dermatology
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Mycobacterial antigen(s) induce anergy by altering TCR- and TCR/CD28-induced signalling events: insights into T-cell unresponsiveness in leprosy.

2009

Present study investigates the role of Mycobacterium leprae (M. leprae) antigens on TCR- and TCR/CD28-induced signalling leading to T-cell activation and further correlates these early biochemical events with T-cell anergy, as prevailed in advanced stages of leprosy. We observed that both whole cell lystae (WCL) and soluble fraction of M. leprae sonicate (MLSA) not only inhibited TCR, thapsigargin and ionomycin induced calcium fluxes by diminishing the opening of calcium channels, but also TCR- or TCR/CD28-induced proximal signalling events like phosphorylation of Zap-70 and protein kinase-C (PKC) activity. Study of TCR- and TCR/CD28-induced downstream signals revealed that M. leprae antige…

Antigens Differentiation T-LymphocyteMAP Kinase Signaling SystemT cellT-LymphocytesImmunologyReceptors Antigen T-Cellchemical and pharmacologic phenomenaBiologyLymphocyte ActivationJurkat cellsp38 Mitogen-Activated Protein Kinaseschemistry.chemical_compoundJurkat CellsCD28 AntigensAntigens CDLeprosyCalcium fluxmedicineHumansLectins C-TypeEnzyme InhibitorsPromoter Regions GeneticMolecular BiologyMycobacterium lepraeProtein Kinase CCell ProliferationClonal AnergyAntigens BacterialMitogen-Activated Protein Kinase 3ZAP-70 Protein-Tyrosine KinaseIonophoresNFATC Transcription FactorsIonomycinT-cell receptorInterleukin-2 Receptor alpha SubunitCD28hemic and immune systemsNFATbiology.organism_classificationCell biologyMycobacterium lepraemedicine.anatomical_structurechemistryGene Expression RegulationIonomycinImmunologyInterleukin-2ThapsigarginCalciumMolecular immunology
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To the research of treatments for the typical calcific disease of old aortic valve in the omics era: Is the miR-195 a therapeutic signature via targe…

2020

Calcific aortic valve disease (CAVD) is the most frequent form of val-vular pathology [1,2], with high percentages of mortality and morbidityin Western populations, so much to be a very public health problem [2].Diverse millions of subjects are affected by CAVD and the major numberare old individuals (65- older), even if some have a younger age and aregenerally affected by congenital bicuspid aortic valve (BAV) disease[2,3]. CAVD in BAV individuals arises decades earlier respect to subjectswith the physiological tricuspid aortic valve [3]. Furthermore, it can leadto death if untreated with surgical aortic valve replacement or trans-catheter aortic valve implantation, its unique treatments […

Aortic valvemedicine.medical_specialtybicuspid aortic valvebusiness.industryp38 mitogen-activated protein kinasesDiseasemedicine.diseaseOmicsBicuspid aortic valvemedicine.anatomical_structuremiR-195Internal medicinemedicineCardiologyCardiology and Cardiovascular Medicinebusiness
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DNA replication arrest in response to genotoxic stress provokes early activation of stress-activated protein kinases (SAPK/JNK).

2009

Abstract The impact of DNA damage-induced replication blockage for early activation of stress kinases [stress-activated protein kinase (SAPK)/c-Jun N-terminal kinase (JNK)] is largely unknown. Here, we show that induction of dual phosphorylation of SAPK/JNK by the DNA polymerase inhibitor aphidicolin was not ameliorated by additional exposure to ultraviolet (UV) light, indicating that overlapping mechanisms participate in signaling to SAPK/JNK triggered by both agents. UV-induced DNA replication blockage, cyclobutane pyrimidine dimer formation and DNA strand break induction coincided with SAPK/JNK phosphorylation at early (≤ 30 min) but not late (≥ 2 h) time points after exposure. Genotoxin…

AphidicolinDNA ReplicationDNA damageUltraviolet RaysPoly ADP ribose polymeraseCell Linechemistry.chemical_compoundMiceAphidicolinStructural BiologyCricetinaeAnimalsHumansLymphocytesPhosphorylationProtein kinase AMolecular BiologyNucleic Acid Synthesis InhibitorsBRCA2 ProteinMice KnockoutbiologyKinaseCell CycleDNA replicationJNK Mitogen-Activated Protein KinasesFibroblastsMolecular biologyProliferating cell nuclear antigenDNA-Binding ProteinsEnzyme ActivationchemistryPyrimidine Dimersbiology.proteinPhosphorylationApoptosis Regulatory ProteinsDNA DamageJournal of molecular biology
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Different muscarinic receptor subtypes modulate proliferation of primary human detrusor smooth muscle cells via Akt/PI3K and map kinases.

2013

While acetylcholine (ACh) and muscarinic receptors in the bladder are mainly known for their role in the regulation of smooth muscle contractility, in other tissues they are involved in tissue remodelling and promote cell growth and proliferation. In the present study we have used primary cultures of human detrusor smooth muscle cells (HDSMCs), in order to investigate the role of muscarinic receptors in HDSMC proliferation. Samples were obtained as discarded tissue from men >65 years undergoing radical cystectomy for bladder cancer and cut in pieces that were either immediately frozen or placed in culture medium for the cell culture establishment. HDSMCs were isolated from samples, propagat…

AtropineMalePyrrolidinesMessenger030232 urology & nephrologyGene ExpressionPhosphatidylinositol 3-Kinases0302 clinical medicineAged Atropine; pharmacology Benzofurans; pharmacology Carbachol; pharmacology Cell Proliferation Cells; Cultured Cholinergic Agonists; pharmacology Gene Expression Humans Male Mitogen-Activated Protein Kinases; metabolism Muscarinic Antagonists; pharmacology Myocytes; Smooth Muscle; metabolism Phosphatidylinositol 3-Kinases; metabolism Piperidines; pharmacology Pirenzepine; analogs /&/ derivatives/pharmacology Proto-Oncogene Proteins c-akt; metabolism Pyrrolidines; pharmacology RNA; Messenger; metabolism Receptors; Muscarinic; physiology Urinary Bladder; cytologyPiperidinesSmooth MuscleReceptorsMuscarinic acetylcholine receptor M5Muscarinic acetylcholine receptorCells CulturedCulturedMuscarinic acetylcholine receptor M3Muscarinic acetylcholine receptor M2Smooth muscle contractionMuscarinic acetylcholine receptor M1Receptors Muscarinic030220 oncology & carcinogenesisMitogen-Activated Protein KinasesAcetylcholinemedicine.drugmedicine.medical_specialtyCarbacholCellsMyocytes Smooth MuscleUrinary BladderMuscarinic AntagonistsBiologyCholinergic Agonists03 medical and health sciencesInternal medicineMuscarinicmedicineHumansRNA MessengerAgedBenzofuransCell ProliferationPharmacologyMyocytesPirenzepineEndocrinologyphysiologycytologyRNACarbacholanalogs /&/ derivatives/pharmacologymetabolismProto-Oncogene Proteins c-aktPharmacological research
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N-acetyl-L-cysteine (NAC) inhibit mucin synthesis and pro-inflammatory mediators in alveolar type II epithelial cells infected with influenza virus A…

2011

64% of chronic obstructive pulmonary disease (COPD) exacerbations are caused by respiratory infections including influenza (strains A and B) and respiratory syncytial virus (RSV). They affect the airway epithelium increasing inflammatory and apoptosis events through mechanisms involving ROS generation, and induce the release of mucins from epithelial cells that are involved in the deterioration of the patient's health during the course of the disease. The antioxidant NAC has proved useful in the management of COPD reducing symptoms, exacerbations and accelerated lung function decline. It has been shown to inhibit influenza virus replication and to diminish the release of inflammatory and ap…

BiologyMucin 5ACmedicine.disease_causeVirus ReplicationBiochemistryp38 Mitogen-Activated Protein KinasesVirusCell LinePulmonary Disease Chronic ObstructivemedicineHumansInterleukin 8PhosphorylationPharmacologyA549 cellMucinNF-kappa BAcetylcysteineRespiratory Syncytial VirusesPulmonary AlveoliInfluenza B virusRespiratory syncytial virus (RSV)Viral replicationApoptosisInfluenza A virusImmunologyRespiratory epitheliumInflammation MediatorsBiochemical pharmacology
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