Search results for "STAT3 Transcription Factor"

showing 10 items of 82 documents

Down-regulation of human CYP3A4 by the inflammatory signal interleukin-6: molecular mechanism and transcription factors involved.

2002

The hepatic drug-metabolizing cytochrome P-450 (CYP) enzymes are down-regulated during inflammation. In vitro studies with hepatocytes have shown that the cytokines released during inflammatory responses are largely responsible for this CYP repression. However, the signaling pathways and the cytokine-activated factors involved remain to be properly identified. Our research has focused on the negative regulation of CYP3A4 (the major drug-metabolizing human CYP) by interleukin 6 (IL-6) (the principal regulator of the hepatic acute-phase response). CYP3A4 down-regulation by IL-6 requires activation of the glycoprotein receptor gp130; however, it does not proceed through the JAK/STAT pathway, a…

MAPK/ERK pathwaySTAT3 Transcription FactorMAP Kinase Signaling Systemp38 mitogen-activated protein kinasesDown-RegulationBiologyBiochemistryTransactivationCytochrome P-450 Enzyme SystemAntigens CDGeneticsCCAAT-Enhancer-Binding Protein-alphaCytokine Receptor gp130Tumor Cells CulturedCytochrome P-450 CYP3AHumansRNA MessengerSTAT3Molecular BiologyTranscription factorCells CulturedMembrane GlycoproteinsDose-Response Relationship DrugInterleukin-6Reverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding Protein-betaJAK-STAT signaling pathwayProtein-Tyrosine KinasesGlycoprotein 130Molecular biologyDNA-Binding ProteinsGene Expression Regulationbiology.proteinHepatocytesTrans-ActivatorsSignal transductionBiotechnologyAcute-Phase ProteinsSignal TransductionTranscription FactorsFASEB journal : official publication of the Federation of American Societies for Experimental Biology
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The STAT3 Inhibitor Galiellalactone Reduces IL6-Mediated AR Activity in Benign and Malignant Prostate Models

2018

IL6/STAT3 signaling is associated with endocrine therapy resistance in prostate cancer, but therapies targeting this pathway in prostate cancer were unsuccessful in clinical trials so far. The mechanistic explanation for this phenomenon is currently unclear; however, IL6 has pleiotropic effects on a number of signaling pathways, including the androgen receptor (AR). Therefore, we investigated IL6-mediated AR activation in prostate cancer cell lines and ex vivo primary prostate tissue cultures in order to gain a better understanding on how to inhibit this process for future clinical trials. IL6 significantly increased androgen-dependent AR activity in LNCaP cells but importantly did not infl…

Male0301 basic medicineCancer ResearchINTERLEUKIN-6LactonesProstate cancerLIGAND-INDEPENDENT ACTIVATION0302 clinical medicineProstateDEPRIVATIONANDROGEN RECEPTORGLUCOCORTICOID-RECEPTORmedicine.anatomical_structureOncologyReceptors Androgen030220 oncology & carcinogenesisAndrogensSILTUXIMAB CNTO 328GROWTHSIGNAL TRANSDUCERSignal transductionLife Sciences & BiomedicineProtein BindingSignal TransductionSTAT3 Transcription FactorENZALUTAMIDEmedicine.drug_classMice NudeModels BiologicalTMPRSS203 medical and health sciencesProtein DomainsCell Line TumorLNCaPmedicineAnimalsHumansCastrationCANCER CELLSScience & TechnologyInterleukin-6business.industryProstatic NeoplasmsDNAmedicine.diseaseAndrogenXenograft Model Antitumor AssaysAndrogen receptor030104 developmental biologyCancer researchbusinessEx vivo
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IL-6 receptor independent stimulation of human gp130 by viral IL-6.

2000

Abstract The genome of human herpes virus 8, which is associated with Kaposi’s sarcoma, encodes proteins with similarities to cytokines and chemokines including a homologue of IL-6. Although the function of these viral proteins is unclear, they might have the potential to modulate the immune system. For viral IL-6 (vIL-6), it has been demonstrated that it stimulates IL-6-dependent cells, indicating that the IL-6R system is used. IL-6 binds to IL-6R, and the IL-6/IL-6R complex associates with gp130 which dimerizes and initiates intracellular signaling. Cells that only express gp130 but no IL-6R cannot be stimulated by IL-6 unless a soluble form of the IL-6R is present. This type of signaling…

MaleSTAT3 Transcription FactorChemokinemedicine.medical_treatmentImmunologyGenetic VectorsBiologylaw.inventionViral ProteinsImmune systemlawAntigens CDmedicineCytokine Receptor gp130Tumor Cells CulturedImmunology and AllergyAnimalsChemical PrecipitationHumansCloning MolecularPhosphorylationInterleukin 6Sarcoma KaposiAgedMembrane GlycoproteinsInterleukin-6Glycoprotein 130Receptors Interleukin-6Growth InhibitorsRecombinant ProteinsCell biologyDNA-Binding ProteinsCytokineInterleukin-6 receptorCOS CellsRecombinant DNAbiology.proteinTrans-ActivatorsIntracellularProtein BindingSignal TransductionJournal of immunology (Baltimore, Md. : 1950)
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In vivo GSH depletion induces c-myc expression by modulation of chromatin protein complexes.

2009

Abstract We hypothesize that glutathione (GSH) fluctuations could have a prominent role in the modulation of c-myc expression through a mechanism affecting chromatin remodeling complexes. This could lead to an open chromatin structure accessible to transcription factors. We studied the in vivo effect of GSH depletion on these complexes bound to the c-myc promoter in the liver of l-buthionine-(S,R)-sulfoximine (BSO)-treated rats. Using chromatin immunoprecipitation we found that 3 h after BSO treatment the repressing complexes Id2 and Sin3A (part of a histone–deacetylase complex) were released from the c-myc promoter. STAT3 was phosphorylated and associated with its coactivator p300 with int…

MaleSTAT3 Transcription FactorTranscriptional ActivationTime FactorsBiologyBiochemistryChromatin remodelingHistone DeacetylasesProto-Oncogene Proteins c-mycHistone H3Physiology (medical)Gene expressionCoactivatorTranscriptional regulationAnimalsp300-CBP Transcription FactorsPhosphorylationRats WistarTranscription factorButhionine SulfoximineInhibitor of Differentiation Protein 2AcetylationChromatin Assembly and DisassemblyMolecular biologyGlutathioneChromatinRatsRepressor ProteinsSin3 Histone Deacetylase and Corepressor ComplexGene Expression RegulationLiverChromatin immunoprecipitationProtein BindingFree radical biologymedicine
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Anti-inflammatory and joint protective effects of extra-virgin olive-oil polyphenol extract in experimental arthritis

2014

The consumption of extra virgin olive oil (EVOO) in Mediterranean countries has shown beneficial effects. A wide range of evidence indicates that phenolic compounds present in EVOO are endowed with anti-inflammatory properties. In this work, we evaluated the effects of EVOO-polyphenol extract (PE) in a model of rheumatoid arthritis, the collagen-induced arthritis model in mice. On day 0, DBA-1/J mice were immunized with bovine type II collagen. On day 21, mice received a booster injection. PE (100 and 200 mg/kg) was orally administered once a day from days 29 to 41 to arthritic mice. We have demonstrated that PE decreases joint edema, cell migration, cartilage degradation and bone erosion. …

MaleSTAT3 Transcription Factormedicine.drug_classEndocrinology Diabetes and Metabolismmedicine.medical_treatmentClinical BiochemistryAnti-Inflammatory AgentsType II collagenAdministration OralDown-RegulationArthritisPharmacologyp38 Mitogen-Activated Protein KinasesBiochemistryDinoprostoneAnti-inflammatoryProinflammatory cytokineMiceEdemamedicineAnimalsPlant OilsPhosphorylationProstaglandin E2Olive OilMolecular BiologyProstaglandin-E SynthasesActivating Transcription Factor 3Nutrition and DieteticsChemistryJNK Mitogen-Activated Protein KinasesNF-kappa BPolyphenolsmedicine.diseaseArthritis ExperimentalIntramolecular OxidoreductasesCyclooxygenase 2Mice Inbred DBARheumatoid arthritisImmunologyCytokinesmedicine.symptomSignal TransductionProstaglandin Emedicine.drugThe Journal of Nutritional Biochemistry
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The interleukin (IL)-31/IL-31R axis contributes to tumor growth in human follicular lymphoma

2014

Interleukin (IL)-31A binds to an heterodimer composed of IL-31 receptor A (IL-31RA) and Oncostatin M Receptor (OSMR). The IL-31/IL-31R complex is involved in the pathogenesis of various skin diseases, including cutaneous T-cell lymphoma. No information is available on the relations between the IL-31/IL-31R complex and B-cell lymphoma. Here we have addressed this issue in follicular lymphoma (FL), a prototypic germinal center(GC)-derived B-cell malignancy. IL-31 enhanced primary FL cell proliferation through IL-31R-driven signal transducer and activator of transcription factor 1/3 (STAT1/3), extracellular signal-regulated kinase 1/2 (ERK1/2) and Akt phosphorylation. In contrast, GC B cells d…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCancer ResearchPrimary Cell CultureFollicular lymphomaBiologyParacrine signallingCytosolCell-Derived MicroparticlesInternal medicinemedicineHumansProtein IsoformsPhosphorylationAutocrine signallingLymphoma FollicularCell ProliferationMitogen-Activated Protein Kinase 1B-LymphocytesMitogen-Activated Protein Kinase 3Gene Expression Regulation LeukemicInterleukinsMicrovesicleMedicine (all)Cell MembraneB-LymphocyteGerminal centerOncostatin M receptorInterleukinProtein IsoformReceptors InterleukinHematologyInterleukinMiddle Agedmedicine.diseaseGerminal CenterMolecular biologyCell-Derived MicroparticleEndocrinologySTAT1 Transcription FactorAnesthesiology and Pain MedicineOncologyFemaleSignal transductionNeoplasm GradingProto-Oncogene Proteins c-aktHumanSignal Transduction
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Extracellular Nampt promotes macrophage survival via a nonenzymatic interleukin-6/STAT3 signaling mechanism.

2008

Macrophages play key roles in obesity-associated pathophysiology, including inflammation, atherosclerosis, and cancer, and processes that affect the survival-death balance of macrophages may have an important impact on obesity-related diseases. Adipocytes and other cells secrete a protein called extracellular nicotinamide phosphoribosyltransferase (eNampt; also known as pre-B cell colony enhancing factor or visfatin), and plasma levels of eNampt increase in obesity. Herein we tested the hypothesis that eNampt could promote cell survival in macrophages subjected to endoplasmic reticulum (ER) stress, a process associated with obesity and obesity-associated diseases. We show that eNampt potent…

MaleSTAT3 Transcription Factormedicine.medical_specialtyCell SurvivalNicotinamide phosphoribosyltransferaseApoptosisBiologyEndoplasmic ReticulumBiochemistryStat3 Signaling Pathwaychemistry.chemical_compoundParacrine signallingMicePiperidinesInternal medicinemedicineAnimalsSecretionAutocrine signallingSTAT3Nicotinamide PhosphoribosyltransferaseMolecular BiologyNicotinamide MononucleotideNicotinamide mononucleotideAcrylamidesInterleukin-6MacrophagesMechanisms of Signal TransductionCell BiologyCell biologyMice Inbred C57BLEndocrinologychemistryGene Expression Regulationbiology.proteinCytokinesSignal transductionSignal TransductionThe Journal of biological chemistry
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Interruption of Macrophage-Derived IL-27(p28) Production by IL-10 during Sepsis Requires STAT3 but Not SOCS3

2014

Abstract Severe sepsis and septic shock are leading causes of morbidity and mortality worldwide. Infection-associated inflammation promotes the development and progression of adverse outcomes in sepsis. The effects of heterodimeric IL-27 (p28/EBI3) have been implicated in the natural course of sepsis, whereas the molecular mechanisms underlying the regulation of gene expression and release of IL-27 in sepsis are poorly understood. We studied the events regulating the p28 subunit of IL-27 in endotoxic shock and polymicrobial sepsis following cecal ligation and puncture. Neutralizing Abs to IL-27(p28) improved survival rates, restricted cytokine release, and reduced bacterial burden in C57BL/…

MaleSTAT3 Transcription Factormedicine.medical_treatmentImmunologySuppressor of Cytokine Signaling ProteinsInflammationSpleenBiologyArticleSepsisMiceSepsismedicineAnimalsHumansImmunology and AllergyReceptors CytokineAntibodies BlockingCecumCells CulturedMice KnockoutSeptic shockInterleukinsMacrophagesReceptors Interleukinmedicine.diseaseBacterial LoadInterleukin-10Mice Inbred C57BLToll-Like Receptor 4Adaptor Proteins Vesicular TransportDisease Models AnimalOxidative StressInterleukin 10Cytokinemedicine.anatomical_structureIntegrin alpha MSuppressor of Cytokine Signaling 3 ProteinMyeloid Differentiation Factor 88ImmunologyTLR4biology.proteinmedicine.symptomJournal of Immunology
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Interleukin (IL)-22 receptor 1 is over-expressed in primary Sjogren's syndrome and Sjögren-associated non-Hodgkin lymphomas and is regulated by IL-18.

2015

Summary The aim of this study was to elucidate more clearly the role of interleukin (IL)-18 in modulating the IL-22 pathway in primary Sjögren's syndrome (pSS) patients and in pSS-associated lymphomas. Minor salivary glands (MSGs) from patients with pSS and non-specific chronic sialoadenitis (nSCS), parotid glands biopsies from non-Hodgkin lymphomas (NHL) developed in pSS patients, were evaluated for IL-18, IL-22, IL-22 receptor 1 (IL-22R1), IL-22 binding protein (IL-22BP) and signal transducer and activator of transcription-3 (STAT-3) expression. MSGs IL-22R1-expressing cells were characterized by confocal microscopy and flow cytometry in pSS, nSCS and healthy controls. The effect of recom…

MaleSalivary Glandslaw.inventionInterleukin 22lawIL-22Immunology and AllergyMyeloid CellsIL-22R1Receptormedicine.diagnostic_testnon-Hodgkin lymphomaLymphoma Non-HodgkinInterleukin-17TranslationalInterleukin-18Lacrimal ApparatusInterleukinMiddle AgedHaematopoiesisSjogren's SyndromeIL-22BPRecombinant DNASjögren's syndromeInterleukin 18FemaleIL-18Signal TransductionAdultSTAT3 Transcription FactorImmunologyPrimary Cell CultureBiologyPeripheral blood mononuclear cellIL-18; IL-22; IL-22BP; IL-22R1; Sjögren's syndrome; non-Hodgkin lymphomaSialadenitisFlow cytometrystomatognathic systemmedicineHumansAgedInterleukinsMacrophagesReceptors InterleukinSettore MED/16 - Reumatologiastomatognathic diseasesGene Expression RegulationImmunologyLeukocytes MononuclearClinical and experimental immunology
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Pancreatic T cell protein-tyrosine phosphatase deficiency ameliorates cerulein-induced acute pancreatitis.

2014

Background Acute pancreatitis (AP) is a common clinical problem whose incidence has been progressively increasing in recent years. Onset of the disease is trigged by intra-acinar cell activation of digestive enzyme zymogens that induce autodigestion, release of pro-inflammatory cytokines and acinar cell injury. T-cell protein tyrosine phosphatase (TCPTP) is implicated in inflammatory signaling but its significance in AP remains unclear. Results In this study we assessed the role of pancreatic TCPTP in cerulein-induced AP. TCPTP expression was increased at the protein and messenger RNA levels in the early phase of AP in mice and rats. To directly determine whether TCPTP may have a causal rol…

MessengerWistarProtein tyrosine phosphataseInbred C57BLBiochemistryOral and gastrointestinalSTAT3Mice2.1 Biological and endogenous factorsPhosphorylationAetiologySTAT3Non-Receptor Type 2CeruletideCancerMice KnockoutProtein Tyrosine Phosphatase Non-Receptor Type 2Pancreatitis Acute NecrotizingNF-kappa B3. Good healthAcute NecrotizingAmylasesTumor necrosis factor alphaTCPTPCell activationCeruletideSTAT3 Transcription Factormedicine.medical_specialtyBiochemistry & Molecular BiologyKnockoutBiologyProinflammatory cytokinePancreatic CancerRare DiseasesInternal medicineAcinar cellmedicineGeneticsAnimalsRNA MessengerRats WistarMolecular BiologyInflammationTumor Necrosis Factor-alphaInterleukin-6ResearchCell BiologyLipaseNFKB1RatsAcute pancreatitisMice Inbred C57BLEndocrinologyPancreatitisbiology.proteinRNAProtein Tyrosine PhosphataseBiochemistry and Cell BiologyDigestive DiseasesKnockout mice
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