Search results for "PROTEIN KINASES"

showing 10 items of 427 documents

Post-Transcriptional Regulation of Human Inducible Nitric-Oxide Synthase Expression by the Jun N-terminal Kinase

2007

Human inducible nitric-oxide synthase (iNOS) expression is regulated both at transcriptional and post-transcriptional levels. In the present study, the effect of Jun N-terminal kinase (JNK) on human iNOS expression was investigated. In A549/8 human alveolar epithelial cells, both the inhibition of JNK by a pharmacological inhibitor anthra[1,9-cd]pyrazol-6(2H)-one1,9-pyrazoloanthrone (SP600125) and small interfering RNA (siRNA)-mediated down-regulation of JNK led to a reduction of iNOS mRNA and protein expression. iNOS promoter activity was not affected by these treatments. Hence, JNK seems to regulate iNOS expression through post-transcriptional mechanisms by stabilizing iNOS mRNA. Our labo…

Small interfering RNARNA Stabilityp38 mitogen-activated protein kinasesDown-RegulationNitric Oxide Synthase Type IIRNA-binding proteinNitric Oxidep38 Mitogen-Activated Protein KinasesGene Expression Regulation EnzymologicCell LineTristetraprolinHumansPhosphorylationRNA Small InterferingPromoter Regions GeneticPost-transcriptional regulationAnthracenesPharmacologyRegulation of gene expressionMessenger RNAbiologyChemistryKinaseJNK Mitogen-Activated Protein KinasesEpithelial Cellsrespiratory systemMolecular biologyPulmonary AlveoliNitric oxide synthasebiology.proteinCytokinesMolecular MedicineSignal TransductionMolecular Pharmacology
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Response of yeast cells to high glucose involves molecular and physiological differences when compared to other osmostress conditions.

2015

Yeast cells can be affected by several causes of osmotic stress, such as high salt, sorbitol or glucose concentrations. The last condition is particularly interesting during natural processes where this microorganism participates. Response to osmostress requires the HOG (High Osmolarity Glycerol) pathway and several transcription factors, including Hot1, which plays a key role in high glucose concentrations. In this work, we describe how the yeast response to osmotic stress shows differences in accordance with the stress agent responsible for it. Compared with other conditions, under high glucose stress, delocalization of MAPK (Mitogen-Activated Protein Kinase) Hog1 is slower, induction of …

Snf3Saccharomyces cerevisiae ProteinsOsmotic shockTranscription GeneticSaccharomyces cerevisiaeChitinSaccharomyces cerevisiaeOsmosisApplied Microbiology and BiotechnologyMicrobiologychemistry.chemical_compoundOsmotic PressureGene Expression Regulation FungalSorbitolProtein kinase AbiologyGlycogenEthanolBenzenesulfonatesOsmolar ConcentrationGeneral Medicinebiology.organism_classificationYeastDNA-Binding ProteinsRepressor ProteinsBasic-Leucine Zipper Transcription FactorsGlucosechemistryBiochemistrySorbitolMitogen-Activated Protein KinasesTranscription FactorsFEMS yeast research
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Molecular mechanisms of sorafenib action in liver cancer cells.

2012

Sorafenib, a multikinase inhibitor, recently received FDA approval for the treatment of advanced hepatocellular carcinoma (HCC). However, as the clinical application of sorafenib evolves, there is increasing interest in defining the mechanisms underlying its anti-tumor activity. Considering that this specific inhibitor could target unexpected molecules depending on the biologic context, a precise understanding of its mechanism of action could be critical to maximize its treatment efficacy, while minimizing adverse effects. Two human HCC cell lines (HepG2 and Huh7), carrying different biological and genetic characteristics, were used in this study to examine the intracellular events leading …

SorafenibDNA ReplicationNiacinamideCarcinoma HepatocellularDNA RepairTranscription GeneticAngiogenesisCell SurvivalPyridinesApoptosisPharmacologyBiologysorafenib HCC mini-chromosome maintenance genes Dickkopf1 Harakiri Acheron/LARP6 YAP1 cell cycle microarray global gene expression analysisCell Line TumormedicineCell AdhesionHumansneoplasmsMolecular BiologyProtein Kinase InhibitorsCell ProliferationYAP1Neovascularization PathologicCell growthGene Expression ProfilingPhenylurea CompoundsBenzenesulfonatesCell CycleLiver NeoplasmsBiological TransportCell BiologyCell cycleSorafenibmedicine.diseasedigestive system diseasesMechanism of actionHepatocellular carcinomaProtein Biosynthesismedicine.symptomMitogen-Activated Protein KinasesLiver cancerDevelopmental Biologymedicine.drugSignal Transduction
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p38 MAPK activation is required for Paracentrotus lividus skeletogenesis

2008

We investigated the p38 MAPK role during sea urchin, Paracentrotus lividus, development. We found that at the morula stage, before the onset of skeletogenesis, p38 MAPK shows a peak of activity, and we tested whether p38 MAPK activity has any effect on skeletogenesis. By immunohistochemistry on whole-mount embryos we show the preferential localization of the active p38 form both in the presumptive PMCs and bilateral spiculo- genesis centers in control embryos, and in the radialized supernumerary spiculogenesis centers induced by NiCl2 treatment. By using SB203580, a p38 MAPK specific inhibitor, we show that p38 activity is required both for the initial triradiate spicule rudiments formation…

Spiculeanimal structuresbiologyp38 mitogen-activated protein kinasesEmbryoAnatomyp38 MAPKbiology.organism_classificationSB203580Paracentrotus lividusCell biologyskeletogenesissea urchin developmentbiology.animalembryonic structuresGeneticsImmunohistochemistryp38 MAPK; SB203580; sea urchin development; skeletogenesisGeneral Agricultural and Biological SciencesSea urchin
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Oleuropein protects against dextran sodium sulfate-induced chronic colitis in mice.

2013

The anti-inflammatory effect of oleuropein (1), the major phenolic secoiridoid in Olea europaea, was evaluated in an experimental model of chronic colitis in mice. Animals were exposed to four repeated cycles of dextran sodium sulfate in drinking water followed by a 7-day rest period. Animals receiving a standard diet supplemented with 0.25% of 1 (equivalent to 500 mg/kg/day) for 56 days exhibited a decrease of inflammatory symptoms, as reflected by improvement of disease activity index and histopathological changes. It was found that 1 decreased inflammatory cell recruitment and the release of inflammatory cytokines interleukin (IL)-1β and IL-6 with increased IL-10 levels in colon tissue. …

T-LymphocytesInterleukin-1betaIridoid GlucosidesAnti-Inflammatory AgentsPharmaceutical ScienceNitric Oxide Synthase Type IIPharmacologyp38 Mitogen-Activated Protein KinasesAnalytical Chemistrychemistry.chemical_compoundMiceOleuropeinOleaDrug DiscoveryAnimalsIridoidsIntestinal MucosaChronic colitisPyransPharmacologybiologyMolecular StructureExperimental modelInterleukin-6Organic ChemistryDextran Sulfatebiology.organism_classificationColitisInterleukin-10Mice Inbred C57BLComplementary and alternative medicinechemistryOleaCyclooxygenase 2Molecular MedicineDextran sodium sulfateJournal of natural products
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Hematopoietic stem cell quiescence and function are controlled by the CYLD–TRAF2–p38MAPK pathway

2015

Tesio at al. identify a novel pathway controlled by the tumor suppressor and deubiquitinase cylindromatosis (CYLD), which is involved in the regulation of hematopoietic stem cell quiescence and repopulation potential.

TRAF2Tumor suppressor geneMAP Kinase Signaling SystemImmunologyRegulatorBiologyp38 Mitogen-Activated Protein KinasesArticleMicemedicineAnimalsImmunology and AllergyMice KnockoutRegulation of gene expressionNF-kappa BHematopoietic stem cellCell BiologyHematopoietic Stem CellsTNF Receptor-Associated Factor 2PhenotypeDeubiquitinating Enzyme CYLDCell biologyCysteine EndopeptidasesHaematopoiesismedicine.anatomical_structureGene Expression RegulationMutationStem cellJournal of Experimental Medicine
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Serine- and Threonine/Valine-Dependent Activation of PDK and Tor Orthologs Converge on Sch9 to Promote Aging

2014

Dietary restriction extends longevity in organisms ranging from bacteria to mice and protects primates from a variety of diseases, but the contribution of each dietary component to aging is poorly understood. Here we demonstrate that glucose and specific amino acids promote stress sensitization and aging through the differential activation of the Ras/cAMP/PKA, PKH1/2 and Tor/S6K pathways. Whereas glucose sensitized cells through a Ras-dependent mechanism, threonine and valine promoted cellular sensitization and aging primarily by activating the Tor/S6K pathway and serine promoted sensitization via PDK1 orthologs Pkh1/2. Serine, threonine and valine activated a signaling network in which Sch…

ThreonineCancer ResearchAgingSerineMice0302 clinical medicineSettore BIO/13 - Biologia ApplicataGene Expression Regulation FungalMolecular Cell BiologySerineSignaling in Cellular ProcessesThreonineGenetics (clinical)Cellular Stress Responses0303 health sciencesageing longevity Sch9 Tor Pkhs nutrients amino acidssurvival stress resistanceMechanisms of Signal TransductionValineCell biologyBiochemistryPhosphorylationSignal transductionResearch ArticleSignal TransductionSaccharomyces cerevisiae Proteinslcsh:QH426-470Adenylyl Cyclase Signaling PathwayLongevityP70-S6 Kinase 1Ras SignalingSaccharomyces cerevisiaeBiologyMicrobiologySignaling Pathways3-Phosphoinositide-Dependent Protein Kinases03 medical and health sciencesModel OrganismsStress PhysiologicalGeneticsAnimalsGene NetworksProtein kinase AMolecular BiologyTranscription factorBiologyEcology Evolution Behavior and Systematics030304 developmental biologySerine/threonine-specific protein kinase[SDV.GEN]Life Sciences [q-bio]/GeneticsCyclic AMP-Dependent Protein Kinaseslcsh:GeneticsGlucoseFoodTor SignalingProtein Kinases030217 neurology & neurosurgeryTranscription Factors
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JNK phosphorylation relieves HDAC3-dependent suppression of the transcriptional activity of c-Jun

2003

The AP-1 transcription factor c-Jun is a prototypical nuclear effector of the JNK signal transduction pathway. The integrity of JNK phosphorylation sites at serines 63/73 and at threonines 91/93 in c-Jun is essential for signal-dependent target gene activation. We show that c-Jun phosphorylation mediates dissociation of an inhibitory complex, which is associated with histone deacetylase 3 (HDAC3). The subsequent events that ultimately cause increased mRNA synthesis are independent of c-Jun phosphorylation and its interaction with JNK. These findings provide an 'activation by de-repression' model as an explanation for the stimulatory function of JNK on c-Jun.

ThreonineTranscriptional ActivationTranscription GeneticMAP Kinase Kinase 4Proto-Oncogene Proteins c-junRecombinant Fusion ProteinsMitogen-activated protein kinase kinaseHistone DeacetylasesGeneral Biochemistry Genetics and Molecular BiologyCell LinePhosphorylation cascadeMiceSuppression GeneticGenes ReporterSerineAnimalsHumansRNA MessengerPhosphorylationMolecular BiologyTranscription factorSequence DeletionMitogen-Activated Protein Kinase KinasesGeneral Immunology and MicrobiologybiologyGeneral Neurosciencec-junJNK Mitogen-Activated Protein KinasesArticles3T3 CellsHDAC3Molecular biologyProtein Structure TertiaryMitogen-activated protein kinaseMutationMutagenesis Site-Directedbiology.proteinPhosphorylationSignal transductionProtein BindingThe EMBO Journal
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Ras, Rap, and Rac Small GTP-binding Proteins Are Targets for Clostridium sordellii Lethal Toxin Glucosylation

1996

Lethal toxin (LT) from Clostridium sordellii is one of the high molecular mass clostridial cytotoxins. On cultured cells, it causes a rounding of cell bodies and a disruption of actin stress fibers. We demonstrate that LT is a glucosyltransferase that uses UDP-Glc as a cofactor to covalently modify 21-kDa proteins both in vitro and in vivo. LT glucosylates Ras, Rap, and Rac. In Ras, threonine at position 35 was identified as the target amino acid glucosylated by LT. Other related members of the Ras GTPase superfamily, including RhoA, Cdc42, and Rab6, were not modified by LT. Incubation of serum-starved Swiss 3T3 cells with LT prevents the epidermal growth factor-induced phosphorylation of m…

ThreonineUridine Diphosphate GlucoseRHOABacterial ToxinsMolecular Sequence DataClostridium sordelliimacromolecular substancesCDC42GTPaseBiologyCell morphologyBiochemistryGTP PhosphohydrolasesProto-Oncogene Proteins p21(ras)MiceGTP-binding protein regulatorsGTP-Binding ProteinsAnimalsHumansAmino Acid SequenceMolecular BiologyClostridiumEpidermal Growth FactorKinase3T3 CellsCell Biologybiology.organism_classificationMolecular biologyActinsrac GTP-Binding ProteinsActin CytoskeletonKineticsGlucoserap GTP-Binding ProteinsGlucosyltransferasesCalcium-Calmodulin-Dependent Protein Kinasesbiology.proteinPhosphorylationGuanosine TriphosphateHeLa CellsJournal of Biological Chemistry
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pRb suppresses camptothecin-induced apoptosis in human osteosarcoma Saos-2 cells by inhibiting c-Jun N-terminal kinase

2001

AbstractThis paper studies the cytotoxic effect induced by the topoisomerase I inhibitor camptothecin in human osteosarcoma Saos-2 cells, which lack p53 and contain a non-functional form of the product of the retinoblastoma gene, pRb. Cytotoxicity induced by camptothecin was dose- and time-dependent; the treatment with 100 nM camptothecin reduced cell viability by 50% at 32 h and by 75% at 72 h of exposure. The cytotoxic effect was caused by apoptosis, as ascertained by morphological evidence, acridine orange-ethidium bromide staining and flow cytometric analysis. Apoptosis was accompanied by both the activation of caspase-3 and the fragmentation of poly(ADP-ribose) polymerase. Treatment wi…

Time FactorsCell SurvivalProto-Oncogene Proteins c-junBlotting WesternBiophysicsApoptosisBiologyTransfectionRetinoblastoma ProteinBiochemistryStructural BiologyTumor Cells CulturedpRb JNK topoisomerase I inhibitors osteosarcomaGeneticsmedicineHumansCytotoxic T cellViability assayPhosphorylationFragmentation (cell biology)neoplasmsMolecular BiologySaos-2 cellsc-Jun N-terminal kinaseCell SizeDose-Response Relationship DrugCaspase 3Cell growthCell Cyclec-junJNK Mitogen-Activated Protein KinasesHydrogen PeroxideCell BiologyFlow CytometryGlutathioneMolecular biologyEnzyme ActivationOxidative StresspRbDNA Topoisomerases Type IApoptosisCaspasesCamptothecinMitogen-Activated Protein KinasesPoly(ADP-ribose) PolymerasesTopoisomerase I InhibitorsCamptothecinmedicine.drugFEBS Letters
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