Search results for "PROTEIN KINASES"

showing 10 items of 427 documents

Clostridium difficile toxin A induces expression of the stress-induced early gene product RhoB.

2004

Clostridium difficile toxin A monoglucosylates the Rho family GTPases Rho, Rac, and Cdc42. Glucosylation leads to the functional inactivation of Rho GTPases and causes disruption of the actin cytoskeleton. A cDNA microarray revealed the immediate early gene rhoB as the gene that was predominantly up-regulated in colonic CaCo-2 cells after treatment with toxin A. This toxin A effect was also detectable in epithelial cells such as HT29 and Madin-Darby canine kidney cells, as well as NIH 3T3 fibroblasts. The expression of RhoB was time-dependent and correlated with the morphological changes of cells. The up-regulation of RhoB was approximately 15-fold and was based on the de novo synthesis of …

RHOAPyridinesRHOBBacterial ToxinsClostridium difficile toxin ARAC1GTPaseBiochemistryp38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicGene productEnterotoxinsStress PhysiologicalRhoB GTP-Binding ProteinHumansrhoB GTP-Binding ProteinMolecular BiologyOligonucleotide Array Sequence AnalysisbiologyImidazolesCell BiologyRhoBClostridium difficileActin cytoskeletonMolecular biologyUp-Regulationbiology.proteinGene expressionCaco-2 CellsThe Journal of biological chemistry
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Protein kinase inhibitor β enhances the constitutive activity of G-protein-coupled zinc receptor GPR39.

2014

GPR39 is a G-protein-coupled zinc receptor that protects against diverse effectors of cell death. Its protective activity is mediated via constitutive activation of Gα13 and the RhoA pathway, leading to increased SRE (serum-response element)-dependent transcription; the zinc-dependent immediate activation of GPR39 involves Gq-mediated increases in cytosolic Ca2+ and Gs coupling leading to increased cAMP levels. We used the cytosolic and soluble C-terminus of GPR39 in a Y2H (yeast-2-hybrid) screen for interacting proteins, thus identifying PKIB (protein kinase A inhibitor β). Co-expression of GPR39 with PKIB increased the protective activity of GPR39 via the constitutive, but not the ligand-…

RHOAmedicine.drug_classG proteinCHO CellsBiochemistryCell LineReceptors G-Protein-CoupledMiceCricetulusTwo-Hybrid System TechniquesmedicineAnimalsHumansProtein kinase AReceptorMolecular BiologyProtein Kinase InhibitorsbiologyEffectorCell MembraneIntracellular Signaling Peptides and ProteinsCell BiologyProtein kinase inhibitorCyclic AMP-Dependent Protein KinasesProtein Kinase A InhibitorCytosolZincBiochemistrybiology.proteinHeLa CellsThe Biochemical journal
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Age-dependent regulation of antioxidant genes by p38α MAPK in the liver

2018

p38α is a redox sensitive MAPK activated by pro-inflammatory cytokines and environmental, genotoxic and endoplasmic reticulum stresses. The aim of this work was to assess whether p38α controls the antioxidant defense in the liver, and if so, to elucidate the mechanism(s) involved and the age-related changes. For this purpose, we used liver-specific p38α-deficient mice at two different ages: young-mice (4 months-old) and old-mice (24 months-old). The liver of young p38α knock-out mice exhibited a decrease in GSH levels and an increase in GSSG/GSH ratio and malondialdehyde levels. However, old mice deficient in p38α had higher hepatic GSH levels and lower GSSG/GSH ratio than young p38α knock-…

ROS Reactive oxygen species;RSK1 Ribosomal S6 kinase10301 basic medicineMAPK/ERK pathwayAgingHPLC High-performance liquid chromatographyAntioxidantmedicine.medical_treatmentTBP TATA-binding proteinClinical BiochemistryDEN Diethyl nitrosamine;MKP-1 MAPK phosphatase-1IκB kinaseGCLc Glutamate cysteine ligase catalytic subunitp38 Mitogen-Activated Protein KinasesG6PDH Glucose-6-phosphate dehydrogenaseBiochemistryAntioxidantsMicechemistry.chemical_compoundSuperoxide Dismutase-1Akt Protein kinase B0302 clinical medicineNrf2 Nuclear factor erythroid 2-related factor-2IL InterleukinSOD1 Cu/Zn-superoxide dismutaselcsh:QH301-705.5Mice KnockoutMK2 MAP-activated protein kinase 2;PGC-1α Peroxisome proliferator-activated receptor gamma coactivator 1-alphachemistry.chemical_classificationlcsh:R5-920Trx ThioredoxinGlutathione DisulfideTNF-α Tumor necrosis factor-alphabiologyLPS Lipopolysaccharide;GSSG Oxidized glutathione;MEF Mouse embryonic fibroblastsNF-kappa BGstm1 Glutathione S-transferase mu 1CatalaseEndoplasmic Reticulum StressGlutathioneLiverGSH Reduced glutathione;Catalase030220 oncology & carcinogenesisJNK c-Jun N-terminal kinaselcsh:Medicine (General)Research Papermedicine.medical_specialtyNF-E2-Related Factor 2Glutamate-Cysteine LigaseMKK MAPK kinaseAP-1 Activator protein-1IKK IƙB KinaseGene Expression Regulation EnzymologicSuperoxide dismutase03 medical and health sciencesInternal medicineGlutamate cysteine ligaseEGFR Epidermal growth factor receptormedicineAnimalsNuclear factor ƙBAnd catalaseChIP Chromatin immunoprecipitation;Protein kinase BNF-ƙB Nuclear factor kappa BSuperoxide DismutaseSuperoxide dismutase 1Superoxide dismutase 2Organic ChemistryGlutathioneASK1 Apoptosis signal-regulating kinase 1ATF2 activating transcription factor 2;030104 developmental biologyEndocrinologyEnzymeHsp Heat shock proteinlcsh:Biology (General)chemistrybiology.proteinSOD2 Mn-superoxide dismutaseMAPK mitogen activated protein kinaseNEM N-ethyl maleimide;Redox Biology
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Activation of mitogen-activated protein kinase by the bradykinin B2receptor is independent of receptor phosphorylation and phosphorylation-triggered …

1999

Recent evidence suggests that serine/threonine phosphorylation and internalization of beta2-adrenergic receptors play critical roles in signalling to the mitogen-activated protein kinase cascade. To investigate whether this represents a general mechanism employed by G protein-coupled receptors, we studied the requirement of these processes in the activation of mitogen-activated protein kinase by G alpha(q)-coupled bradykinin B2 receptors. Mutant B2 receptors impaired in receptor phosphorylation and internalization are fully capable to activate mitogen-activated protein kinase. Bradykinin-induced long-term effects on mitogenic signalling monitored by measuring the transcriptional activity of…

Receptor Bradykinin B2Bradykinin B2 receptorBiophysicsMitogen-activated protein kinase kinaseBradykininBiochemistryCell LineMAP2K7Structural BiologyMitogenic signallingGeneticsHumansPhosphorylationBradykinin receptorProtein kinase AMolecular BiologyProtein kinase CG protein-coupled receptorG protein-coupled receptor kinaseMAP kinase kinase kinaseChemistryReceptors BradykininCell BiologyMitogen-activated protein kinaseEnzyme ActivationBiochemistryCalcium-Calmodulin-Dependent Protein KinasesInternalizationSignal TransductionFEBS Letters
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Two distinct Ca2+ influx pathways activated by the bradykinin B2 receptor.

1996

The hormone-induced depletion of cellular Ca stores provides a signal for the Ca2+ influx into electrically non-excitable cells; however, the underlying molecular mechanisms remain elusive. Therefore, we analyzed bradykinin-activated Ca2+ influx into human foreskin fibroblast cells, HF-15, by fura-2 and 45Ca labeling to discriminate between Ca2+ influx into the fura-sensitive compartment and Ca uptake into fura-insensitive Ca stores. Bradykinin-activated CaZt influx into the fura-sensitive compartment was blocked by inhibitors of NO synthases. These inhibitors also suppressed bradykinin-activated increases in cGMP, indicating that the NO-dependent increase in cGMP is involved in the activat…

Receptor Bradykinin B2BradykininBradykininNitric OxideBiochemistryNitric oxideCell Linechemistry.chemical_compoundmedicineCyclic GMP-Dependent Protein KinasesHumansFibroblastCyclic GMPInterphaseFluorescent DyesIon TransportCell growthChemistryKinaseReceptors BradykininCa2 influxCompartment (chemistry)Calcium Channel BlockersCell biologymedicine.anatomical_structureBiochemistryCytoplasmCalciumFura-2Cell DivisionEuropean journal of biochemistry
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Respiration and low cAMP-dependent protein kinase activity are required for high-level expression of the peroxisomal thiolase gene in Saccharomyces c…

1996

Transcription of genes for peroxisomal proteins is repressed by glucose and induced by oleate. At least for the peroxisomal thiolase gene (POT1) there is a third regulatory mechanism, mediated by the transcription factor Adr1p, which is responsible for the high-level expression of the gene in stationary phase. Here we show that a region in the POT1 promoter that extends from positions -238 to -152 mediates this mechanism, and we suggest that Adr1p acts indirectly on POT1. We have also analyzed the role of the cAMP-dependent protein kinase (PKA) in the transcriptional regulation of POT1. PKA exerts a negative control: the high, unregulated PKA activity in a bcy1 mutant maintains POT1 transcr…

Regulation of gene expressionSaccharomyces cerevisiae ProteinsTranscription GeneticThiolaseSaccharomyces cerevisiaeBiologyRegulatory Sequences Nucleic AcidCAMP-dependent protein kinase activityCyclic AMP-Dependent Protein KinasesMicrobodiesMitochondriaDNA-Binding ProteinsFungal ProteinsBiochemistryRegulatory sequenceGene Expression Regulation FungalGeneticsTranscriptional regulationRas2Acetyl-CoA C-AcetyltransferaseProtein kinase APromoter Regions GeneticMolecular BiologyTranscription factorTranscription FactorsMoleculargeneral genetics : MGG
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Effect of LIF-withdrawal on acetylcholine synthesis in the embryonic stem cell line CGR8 is not mediated by STAT3, PI3Ks or cAMP/PKA pathways.

2015

Acetylcholine (ACh) acts as a local cellular signaling molecule and is widely expressed in nature, including mammalian cells and embryonic stem cells. The murine embryonic stem cell line CGR8 synthesizes and releases substantial amounts of ACh. Particularly during early differentiation - a period associated with multiple alterations in geno-/phenotype functions - synthesis and release of ACh are increased by 10-fold. In murine stem cells second messengers of the STAT-3, PI3K and cAMP/PKA pathways are involved in maintaining self-renewal and pluripotency. The present experiments were designed to test whether blockers of these signaling pathways enhance ACh cell content in the presence of LIF…

STAT3 Transcription FactorCell signalingCurcuminMorpholinesImmunologyBiologyLeukemia Inhibitory FactorGene Expression Regulation Enzymologicchemistry.chemical_compoundMicePhosphatidylinositol 3-KinasesCyclic AMPImmunology and AllergyAnimalsLY294002PI3K/AKT/mTOR pathwayEmbryonic Stem CellsPharmacologySulfonamidesForskolinColforsinIsoquinolinesEmbryonic stem cellCyclic AMP-Dependent Protein KinasesAcetylcholineCell biologychemistryChromonesSecond messenger systemSignal transductionStem cellSignal TransductionInternational immunopharmacology
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Decreased SAPK/JNK signalling affects cytokine release and STAT3 activation in psoriatic fibroblasts.

2015

STAT3 Transcription FactorMAP Kinase Signaling Systemmedicine.medical_treatmentDermatologyBiochemistryp38 Mitogen-Activated Protein KinasesPsoriasismedicineSapk jnkHumansPsoriasisPhosphorylationSTAT3Molecular BiologyStat3 activationMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3biologyChemistryInterleukin-6Tumor Necrosis Factor-alphaInterleukin-8JNK Mitogen-Activated Protein KinasesTranscription Factor RelAFibroblastsmedicine.diseaseSignallingCytokineCase-Control StudiesCancer researchbiology.proteinPhosphorylationTumor necrosis factor alphaExperimental dermatology
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Intestinal anti-inflammatory activity of ellagic acid in the acute and chronic dextrane sulfate sodium models of mice colitis.

2013

Abstract Ethnopharmacological relevance Pomegranate (Punica granatum L.; Lythraceae) has traditionally been used for the treatment of various inflammatory diseases, including ulcerative colitis (UC). Because its fruits and extracts are rich in ellagitannins, which release ellagic acid when hydrolyzed, consumption of pomegranate products is currently being widely promoted for their potential health effects, including the prevention of inflammatory diseases and cancer. To evaluate the anti-inflammatory effects of ellagic acid on dextran sulfate sodium (DSS)-induced acute and chronic experimental colitis in two different strains of mice and to elucidate its possible mechanisms of action. Mater…

STAT3 Transcription Factormedicine.drug_classColonp38 mitogen-activated protein kinasesAnti-Inflammatory AgentsPharmacologyp38 Mitogen-Activated Protein KinasesAnti-inflammatoryBALB/cchemistry.chemical_compoundMiceEllagic AcidNF-KappaB Inhibitor alphaDrug DiscoverymedicineAnimalsColitisIntestinal MucosaSTAT3PeroxidasePharmacologyMice Inbred BALB Cbiologybusiness.industryDextran SulfateNF-kappa BCancermedicine.diseasebiology.organism_classificationColitisUlcerative colitisMice Inbred C57BLDisease Models AnimalchemistryImmunologybiology.proteinCytokinesFemaleI-kappa B ProteinsbusinessEllagic acidJournal of ethnopharmacology
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Yeast karyopherins Kap123 and Kap95 are related to the function of the cell integrity pathway

2009

The characterization of mutant strains in the gene encoding karyopherin Kap123 has revealed several morphogenetic defects. Inactivation of KAP123 caused alterations in the actin cytoskeleton, resulting in hyperpolarization and resistance to the actin polymerization inhibitor latrunculin B. In fact, the level of actin filaments is increased in kap123 mutant cells. In addition to the defect in actin cytoskeleton, the kap123 mutant cells showed a weakened cell wall, cell lysis and a growth defect in either the presence of sodium dodecyl sulfate or at high temperatures, which is alleviated by osmotic stabilizers. These defects in cell integrity and the actin cytoskeleton suggested a relationshi…

Saccharomyces cerevisiae ProteinsArp2/3 complexMADS Domain ProteinsSaccharomyces cerevisiaemacromolecular substancesApplied Microbiology and BiotechnologyMicrobiologyGene Knockout TechniquesCell WallNuclear proteinCytoskeletonCytoskeletonProtein kinase CActinMicroscopyMicrobial ViabilitybiologyActin remodelingGeneral Medicinebeta KaryopherinsActin cytoskeletonActinsCell biologybiology.proteinLatrunculinMitogen-Activated Protein KinasesFEMS Yeast Research
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