Search results for "AP-1"

showing 10 items of 47 documents

Resveratrol decreases the levels of miR-155 by upregulating miR-663, a microRNA targeting JunB and JunD.

2010

An inflammatory component is present in the microenvironment of most neoplastic tissues, including those not causally related to an obvious inflammatory process. Several microRNAs, and especially miR-155, play an essential role in both the innate and adaptative immune response. Resveratrol (trans-3,4#,5-trihydroxystilbene) is a natural antioxidant with anti-inflammatory properties that is currently at the stage of preclinical studies for human cancer prevention. Here, we establish that, in human THP-1 monocytic cells as well as in human blood monocytes, resveratrol upregulates miR- 663, a microRNA potentially targeting multiple genes implicated in the immune response. In THP-1 cells, miR-66…

LipopolysaccharidesCancer ResearchJUNBProto-Oncogene Proteins c-junBlotting WesternResveratrolBiologyMonocytesmiR-15503 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemDownregulation and upregulationRNA interferencemicroRNAStilbenesBiomarkers TumorHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLuciferases[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCells Cultured030304 developmental biologyOligonucleotide Array Sequence AnalysisCancer Biology0303 health sciencesInnate immune systemmicroRNAReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingmicroRNA; ResveratrolGeneral MedicineAntineoplastic Agents Phytogenic3. Good healthUp-RegulationTranscription Factor AP-1MicroRNAschemistryGene Expression RegulationResveratrol030220 oncology & carcinogenesisCancer research
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Measles virus enhances the expression of cellular immediate-early genes and DNA-binding of transcription factor AP-1 in lung epithelial A549 cells.

2002

In this work we investigated the effect of measles virus (MV) infection on the expression of immediate-early genes junB, c-jun and c-fos mRNA as well as AP-1 DNA-binding activity in the lung epithelial-like adenocarcinoma cell line A549. The transcription factor AP-1, which is a group of dimeric complexes of the Fos and Jun family proteins, is an important regulator in many cellular responses to different extracellular stimuli. Membrane cofactor protein CD46, which acts as a receptor for laboratory-adapted and vaccine strains of MV, has been reported to associate with beta1 integrin molecules, which are known to trigger signaling events and activate immediate-early genes. The expression of …

Lung NeoplasmsJUNBBiologyMeasles virusMembrane Cofactor Protein03 medical and health sciencesAntigens CDVirologyGene expressionTumor Cells CulturedHumansMononegaviralesTranscription factorGenes Immediate-Early030304 developmental biologyA549 cell0303 health sciencesMembrane GlycoproteinsCD46Interleukin-6030302 biochemistry & molecular biologyGeneral MedicineDNAbiology.organism_classificationVirology3. Good healthTranscription Factor AP-1Gene Expression RegulationMeasles virusImmediate early geneArchives of virology
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Global Functional Analyses of Cellular Responses to Pore-Forming Toxins

2011

Here we present the first global functional analysis of cellular responses to pore-forming toxins (PFTs). PFTs are uniquely important bacterial virulence factors, comprising the single largest class of bacterial protein toxins and being important for the pathogenesis in humans of many Gram positive and Gram negative bacteria. Their mode of action is deceptively simple, poking holes in the plasma membrane of cells. The scattered studies to date of PFT-host cell interactions indicate a handful of genes are involved in cellular defenses to PFTs. How many genes are involved in cellular defenses against PFTs and how cellular defenses are coordinated are unknown. To address these questions, we pe…

MAPK/ERK pathwayTranscription GeneticImmunology/Innate ImmunityMessengerInteractomeInfectious Diseases/Bacterial InfectionsRNA interference2.1 Biological and endogenous factorsAetiologyBiology (General)Genes HelminthCaenorhabditis elegansOligonucleotide Array Sequence AnalysisGenetics0303 health sciencesGenomebiologyReverse Transcriptase Polymerase Chain ReactionGenetics and Genomics/Functional Genomics030302 biochemistry & molecular biologyrespiratory systemCell biologyInfectious DiseasesMedical MicrobiologyRNA InterferenceSignal transductionDNA microarrayTranscriptionBiotechnologyResearch ArticleSignal TransductionPore Forming Cytotoxic ProteinsQH301-705.5Virulence FactorsMAP Kinase Signaling System1.1 Normal biological development and functioningBacterial ToxinsImmunologyMicrobiologyDNA-binding proteinCell Line03 medical and health sciencesBacterial ProteinsGeneticUnderpinning researchVirologyEscherichia coliHelminthGeneticsAnimalsHumansRNA MessengerCaenorhabditis elegansCaenorhabditis elegans ProteinsMolecular BiologyGene030304 developmental biologyGenome HelminthCell MembraneGenetics and GenomicsRC581-607biology.organism_classificationrespiratory tract diseasesTranscription Factor AP-1Emerging Infectious DiseasesGenesRNAParasitologyGeneric health relevanceRNA HelminthImmunologic diseases. AllergyPLoS Pathogens
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Activation of Cardiac c-Jun NH 2 -Terminal Kinases and p38-Mitogen–Activated Protein Kinases With Abrupt Changes in Hemodynamic Load

2001

Abstract —The role of mitogen-activated protein kinase (MAPK) pathways as signal transduction intermediates of hemodynamic stress leading to cardiac hypertrophy in the adult heart is not fully established. In a rat model of pressure-overload hypertrophy, we examined whether activation of MAPK pathways, namely, the extracellular signal–regulated protein kinase (ERK), c-Jun NH 2 -terminal kinase (JNK), and the p38-MAPK pathways, occurs during rapid changes in hemodynamic load in vivo. A slight activation of ERK2 and marked increases in JNK1 and p38-MAPK activities were observed 30 minutes after aortic banding. The increase in p38-MAPK activity was accompanied by an increase in the phosphoryl…

MAPK/ERK pathwaymedicine.medical_specialtyProto-Oncogene Proteins c-junp38 mitogen-activated protein kinasesp38 Mitogen-Activated Protein KinasesVentricular Function LeftStress PhysiologicalInternal medicineInternal MedicinemedicineAnimalsASK1PhosphorylationRats WistarCyclic AMP Response Element-Binding ProteinProtein kinase AProtein kinase CMAPK14Activating Transcription Factor 2biologyKinaseMyocardiumJNK Mitogen-Activated Protein KinasesRatsCell biologyEnzyme ActivationTranscription Factor AP-1Disease Models AnimalEndocrinologyMitogen-activated protein kinasebiology.proteinFemaleMitogen-Activated Protein KinasesTranscription FactorsHypertension
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Aging-induced Up-regulation of Nuclear Binding Activities of Oxidative Stress Responsive NF-kB Transcription Factor in Mouse Cardiac Muscle

1996

The accumulation of lipofuscin to cardiomyocytes is a classical parameter of aging and is believed to reflect oxidative stress. NF-kB transcription factor complex is one of the cellular sensors which responds to oxidative stress and regulates gene expression. Our purpose was to study whether aging affects the level and distribution of DNA binding activities of NF-kB transcription factors both in cardiac sarcoplasm and nuclear extracts. We used electrophoretic mobility shift assays (EMSA) to characterize the DNA binding activities of NF-kB and two other transcription factors. AP-1 and Sp-1, in the myocardium of 4 months and 24 months old male and female NMRI-mice. The protein levels of p50, …

MaleAgingP50Sp1 Transcription FactorSarcoplasmDown-RegulationTranscription factor complexBiologymedicine.disease_causeMiceNF-KappaB Inhibitor alphaGene expressionmedicineAnimalsMolecular BiologyTranscription factorCell NucleusMyocardiumNF-kappa BTranscription Factor RelACardiac muscleNF-kappa B p50 SubunitNF-kappa B p50 SubunitMolecular biologyUp-RegulationDNA-Binding ProteinsTranscription Factor AP-1Oxidative Stressmedicine.anatomical_structureFemaleI-kappa B ProteinsCardiology and Cardiovascular MedicineOxidative stressJournal of Molecular and Cellular Cardiology
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TGF-β Signaling Pathways in Different Compartments of the Lower Airways of Patients With Stable COPD

2017

Background: The expression and localization of transforming growth factor-β (TGF-β) pathway proteins in different compartments of the lower airways of patients with stable COPD is unclear. We aimed to determine TGF-β pathway protein expression in patients with stable COPD. Methods: The expression and localization of TGF-β pathway components was measured in the bronchial mucosa and peripheral lungs of patients with stable COPD (n = 44), control smokers with normal lung function (n = 24), and control nonsmoking subjects (n = 11) using immunohistochemical analysis. Results: TGF-β1, TGF-β3, and connective tissue growth factor expression were significantly decreased in the bronchiolar epithelium…

MaleCCN2 connective tissue growth factorSmad Proteinsairway inflammationCritical Care and Intensive Care MedicineTRAP-1 transforming growth factor-β receptor-associated binding proteinPulmonary Disease Chronic ObstructiveLAP latency-associated peptideSMAD small mother against decapentaplegicBAMBI CTGF SMAD TGF-B airway inflammation autoimmunityLungTGF transforming growth factorLLC large latent complexBAMBI CTGF SMAD TGF-β Airway Inflammation AutoimmunityautoimmunityMiddle Agedrespiratory systemLTBP latent transforming growth factor-β binding proteinImmunohistochemistryTGIF 5′-TG-3′-interacting factorECM extracellular matrixTGFBI transforming growth factor-β-induced proteinFemaleCardiology and Cardiovascular MedicinePI3K phosphoinositide 3-kinaseSignal TransductionTGF-βPulmonary and Respiratory MedicineTGF-βR TGF-β receptorSocio-culturaleBronchiRespiratory MucosaArticleTGF-BTransforming Growth Factor beta1Transforming Growth Factor beta3Macrophages AlveolarHumansAgedBAMBI; CTGF; SMAD; TGF-β; airway inflammation; autoimmunityBAMBIMembrane ProteinsCTGFBMP bone morphogenetic proteinBAMBI; CTG; SMAD; TGF-β; airway inflammation; autoimmunityCTGBAMBI bone morphogenetic proteins and activin membrane-bound inhibitorrespiratory tract diseasesairway inflammation; autoimmunity; BAMBI; CTGF; SMAD; TGF-β; Pulmonary and Respiratory Medicine; Critical Care and Intensive Care Medicine; Cardiology and Cardiovascular MedicineCase-Control StudiesBiomarkersMAPK mitogen-activated protein kinaseSMAD
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Control of Cell Migration and Inflammatory Mediators Production by CORM-2 in Osteoarthritic Synoviocytes

2011

Background Osteoarthritis (OA) is the most widespread degenerative joint disease. Inflamed synovial cells contribute to the release of inflammatory and catabolic mediators during OA leading to destruction of articular tissues. We have shown previously that CO-releasing molecules exert anti-inflammatory effects in animal models and OA chondrocytes. We have studied the ability of CORM-2 to modify the migration of human OA synoviocytes and the production of chemokines and other mediators sustaining inflammatory and catabolic processes in the OA joint. Methodology/Principal Findings OA synoviocytes were stimulated with interleukin(IL)-1β in the absence or presence of CORM-2. Migration assay was…

MaleChemokineAnatomy and PhysiologyInterleukin-1betalcsh:MedicineGene ExpressionMatrix metalloproteinaseBiochemistryCell MovementDrug Discoverylcsh:ScienceMusculoskeletal SystemCells CulturedChemokine CCL2MultidisciplinarybiologyReverse Transcriptase Polymerase Chain ReactionSynovial MembraneNF-kappa BInterleukinCell migrationmedicine.anatomical_structureMedicineFemaleMatrix Metalloproteinase 3Inflammation MediatorsMatrix Metalloproteinase 1Mitogen-Activated Protein KinasesResearch ArticleCell PhysiologyBlotting WesternRheumatologySynovitisOsteoarthritisOrganometallic CompoundsmedicineHumansInterleukin 8BiologyAgedCell ProliferationChemokine CCL20lcsh:RInterleukin-8medicine.diseaseTranscription Factor AP-1CCL20Oxidative StressSmall MoleculesImmunologyCancer researchbiology.proteinlcsh:QSynovial membraneHeme Oxygenase-1PLoS ONE
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Temporal coherency between receptor expression, neural activity and AP-1-dependent transcription regulates Drosophila motoneuron dendrite development.

2013

Neural activity has profound effects on the development of dendritic structure. Mechanisms that link neural activity to nuclear gene expression include activity-regulated factors, such as CREB, Crest or Mef2, as well as activity-regulated immediate-early genes, such as fos and jun. This study investigates the role of the transcriptional regulator AP-1, a Fos-Jun heterodimer, in activity-dependent dendritic structure development. We combine genetic manipulation, imaging and quantitative dendritic architecture analysis in a Drosophila single neuron model, the individually identified motoneuron MN5. First, Dα7 nicotinic acetylcholine receptors (nAChRs) and AP-1 are required for normal MN5 dend…

Mef2Transcriptional ActivationEmbryo NonmammalianTime FactorsTranscription GeneticReceptor expressionReceptors NicotinicCREBSynaptic TransmissionAnimals Genetically ModifiedGenes ReporterCa2+/calmodulin-dependent protein kinaseAnimalsDrosophila ProteinsCholinergic synapseCholinergic neuronMolecular BiologyResearch ArticlesCell NucleusDendritic spikeMicroscopy ConfocalbiologyGene Expression Regulation DevelopmentalDendritesImmunohistochemistryCholinergic NeuronsCell biologyEnzyme ActivationTranscription Factor AP-1Drosophila melanogasterMicroscopy Fluorescencebiology.proteinSignal transductionCalcium-Calmodulin-Dependent Protein Kinase Type 2Developmental BiologySignal TransductionDevelopment (Cambridge, England)
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Suppression of ischemia-induced fos expression and AP-1 activity by an antisense oligodeoxynucleotide to c-fos mRNA.

1994

The molecular events of brain adaptation to injury that may underlie functional recovery after stroke remain largely undefined. Recent observations of altered gene expression in ischemic brain using animal stroke models have opened new avenues for exploration of the biochemical cascades after stroke [1–11]. These postischemic events include an increase in extracellular excitatory amino acid neurotransmitters such as glutamate. Glutamate receptor–mediated activation of phospholipases and protein kinases results in the alteration of nuclear regulatory processes, including the expression of immediate early genes such as c-fos, junB, and c-jun [5, 12]. The Fos, Jun, and JunB proteins have been …

Messenger RNAbiologyBase SequenceJUNBEffectorOligonucleotideMolecular Sequence DataGene ExpressionOligonucleotides Antisensec-FosMolecular biologyReceptor tyrosine kinaseArticleRatsTranscription Factor AP-1NeurologyTranscription (biology)Ischemic Attack TransientGene expressionbiology.proteinAnimalsNeurology (clinical)RNA MessengerProto-Oncogene Proteins c-fosAnnals of neurology
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Hypertrophic agonists induce the binding of c-Fos to an AP-1 site in cardiac myocytes: implications for the expression of GLUT1

2003

Objectives: Serum is among the agents known to induce hypertrophy of cardiac myocytes, which occurs concomitant with an increase in AP-1-mediated transcription. We have examined if this effect correlates with changes in the relative abundance of particular AP-1 heterodimers, as their exact composition under these conditions is unknown. Furthermore, we obtained insight on the specific role of c-Fos from studying the induction of the glucose transporter GLUT1 by serum in fibroblasts. Methods: We characterised the AP-1 heterodimers expressed in neonatal cardiac myocytes by supershift electrophoretic mobility shift assay (EMSA) analysis. Quantitative changes in transcription were measured using…

Monosaccharide Transport ProteinsTranscription GeneticMAP Kinase Signaling SystemPyridinesPhysiologyJUNBBlotting WesternElectrophoretic Mobility Shift Assayc-FosCell LineMicePhysiology (medical)Gene expressionAnimalsMyocyteMyocytes CardiacElectrophoretic mobility shift assayCells CulturedFlavonoidsGlucose Transporter Type 1biologyImidazolesGlucose transporterFibroblastsMolecular biologyRatsEnzyme ActivationTranscription Factor AP-1Animals Newbornbiology.proteinGLUT1Mitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineProto-Oncogene Proteins c-fosGene DeletionProtein BindingFOSBCardiovascular Research
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