Search results for "STAT1"

showing 10 items of 52 documents

Overexpression of STAT-1 by adenoviral gene transfer does not inhibit hepatitis B virus replication.

2006

Objectives Interferons are known to inhibit the replication of hepatitis B viruses (HBV) in several animal models in vitro and in vivo as well in humans. The STAT-1 protein plays a central role in the biological activity of both type I and type II interferons. The lack of functional STAT-1 renders cells and organisms susceptible to bacterial and viral infectious agents. We analysed whether the overexpression of STAT-1 protein enhances the biological interferon response and whether it elicits antiviral acitivity against HBV in vitro. Methods To achieve an efficient STAT-1 overexpression in primary liver cells and hepatoma cells, we generated a recombinant, replication-deficient adenovirus ex…

Hepatitis B virusCarcinoma HepatocellularBlotting WesternGenetic Vectorsmedicine.disease_causeTransfectionVirus ReplicationVirusHepatitis B virus PRE betaAdenoviridaeOrthohepadnavirusInterferonmedicineTumor Cells CulturedAnimalsHumansCells CulturedHepatitis B virusHepatologybiologyLiver NeoplasmsGastroenterologyvirus diseasesHepatitis Bmedicine.diseasebiology.organism_classificationVirologyMolecular biologydigestive system diseasesIn vitroDucksSTAT1 Transcription FactorHepadnaviridaeGene Expression RegulationDNA ViralHepatocytesmedicine.drugEuropean journal of gastroenterologyhepatology
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Interferon-λ and interleukin 22 act synergistically for the induction of interferon-stimulated genes and control of rotavirus infection.

2015

The epithelium is the main entry point for many viruses, but the processes that protect barrier surfaces against viral infections are incompletely understood. Here we identified interleukin 22 (IL-22) produced by innate lymphoid cell group 3 (ILC3) as an amplifier of signaling via interferon-λ (IFN-λ), a synergism needed to curtail the replication of rotavirus, the leading cause of childhood gastroenteritis. Cooperation between the receptor for IL-22 and the receptor for IFN-λ, both of which were 'preferentially' expressed by intestinal epithelial cells (IECs), was required for optimal activation of the transcription factor STAT1 and expression of interferon-stimulated genes (ISGs). These d…

ImmunologyImmunoblottingMolecular Sequence DataGene ExpressionMice Transgenicmedicine.disease_causeRotavirus InfectionsCell LineMadin Darby Canine Kidney CellsInterleukin 22DogsInterferonRotavirusChlorocebus aethiopsmedicineImmunology and AllergyAnimalsHumansSTAT1Intestinal MucosaReceptors CytokineVero CellsMice KnockoutbiologyReverse Transcriptase Polymerase Chain ReactionInterleukinsInnate lymphoid cellInterleukinDrug SynergismEpithelial CellsVirology3. Good healthIntestinesMice Inbred C57BLSTAT1 Transcription FactorViral replicationImmunologybiology.proteinVero cellCytokinesCaco-2 CellsHT29 Cellsmedicine.drugNature immunology
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Cross-Inhibition of Interferon-Induced Signals by GM-CSF Through a Block in Stat1 Activation

2007

We investigated the effects of granulocyte-macrophage colony-stimulating factor (GM-CSF) on biologic signals induced by interferon-alpha (IFN-alpha) and IFN-gamma. In hematopoietic cell lines, IFN-induced signaling was investigated by Western blotting, electrophoretic mobility shift assays (EMSA), flow cytometry, protein-tyrosine phosphatase (PTP) assays, and RT-PCR. GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced Stat1 tyrosine phosphorylation in a time-dependent manner. EMSA showed that GM-CSF inhibited IFN-alpha-induced and IFN-gamma-induced IFN-gamma activator sequence (GAS) binding activity. As a consequence, IFN-induced transcription of the early response gene, IFN-stimulated…

ImmunologyPhosphataseSuppressor of Cytokine Signaling ProteinsProtein tyrosine phosphataseBiologyCell Linechemistry.chemical_compoundVirologyGranulocyte Colony-Stimulating FactorHumansPhosphorylationHistocompatibility Antigens Class IGranulocyte-Macrophage Colony-Stimulating FactorTyrosine phosphorylationDNACell BiologyMolecular biologySTAT1 Transcription FactorIRF1chemistryTyrosine kinase 2PhosphorylationInterleukin-3InterferonsSignal transductionInterferon Regulatory Factor-1Signal TransductionTranscription FactorsProto-oncogene tyrosine-protein kinase SrcJournal of Interferon & Cytokine Research
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STAT1 expression and activation is increased in lesional psoriatic skin

2013

Summary Background  The JAK (Janus kinase)/STAT (signal transducer and activator of transcription) signalling pathway is known to play an important role in many cellular processes including inflammation. The activation of STAT1 is dependent on tyrosine 701 and serine 727 phosphorylation, which leads to the formation of the STAT dimer and modulation of STAT1 activity, respectively. Objective  To determine STAT1 expression and activation in psoriatic skin. Methods  Biopsies were collected from patients with psoriasis. mRNA expression was evaluated by quantitative polymerase chain reaction, whereas the protein and phosphorylation level of STAT1 were evaluated by Western blotting. STAT1 localiz…

Kinasep38 mitogen-activated protein kinasesDermatologyBiologymedicine.diseaseMolecular biologyPsoriasismedicineSTAT proteinbiology.proteinPhosphorylationSTAT1Janus kinaseProtein kinase CBritish Journal of Dermatology
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Cigarette smoke increases BLT2 receptor functions in bronchial epithelial cells: in vitro and ex vivo evidence

2013

Summary Leukotriene B4 (LTB4) is a neutrophil chemotactic molecule with important involvement in the inflammatory responses of chronic obstructive pulmonary disease (COPD). Airway epithelium is emerging as a regulator of innate immune responses to a variety of insults including cigarette smoke, the major risk factor for COPD. In this study we have explored whether cigarette smoke extracts (CSE) or soluble mediators present in distal lung fluid samples (mini-bronchoalveolar lavages) from smokers alter the expression of the LTB4 receptor 2 (BLT2) and peroxisome proliferator-activated receptor-α (PPAR-α) in bronchial epithelial cells. We also evaluated the effects of CSE on the expression of i…

Leukotriene B4NeutrophilsImmunologyIntercellular Adhesion Molecule-1Blotting WesternReceptors Leukotriene B4Peroxisome proliferator-activated receptorSettore MED/41 - AnestesiologiaInflammationBronchiBiologychronic obstructive pulmonary diseasechemistry.chemical_compoundTobaccoacute lung injiurybronchial epithelial cellleukotriene B4.medicineCell AdhesionImmunology and AllergyHumansPPAR alphaReceptorPromoter Regions GeneticCells Culturedchemistry.chemical_classificationInnate immune systemPlant Extractscigarette smokeSmokingEpithelial CellsOriginal Articlesrespiratory systemFlow CytometryIntercellular Adhesion Molecule-1Neutrophiliarespiratory tract diseasesacute lung injiury; bronchial epithelial cells; cigarette smoke; chronic obstructive pulmonary disease; inflammation; leukotriene B4.STAT1 Transcription FactorchemistryinflammationImmunologyRespiratory epitheliumRNA Interferencemedicine.symptomBronchoalveolar Lavage FluidProtein Binding
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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

2009

Cells of the monocyte-macrophage lineage play a central role in the orchestration and resolution of inflammation. Plasticity is a hallmark of mononuclear phagocytes, and in response to environmental signals these cells undergo different forms of polarized activation, the extremes of which are called classic or M1 and alternative or M2. NF-kappaB is a key regulator of inflammation and resolution, and its activation is subject to multiple levels of regulation, including inhibitory, which finely tune macrophage functions. Here we identify the p50 subunit of NF-kappaB as a key regulator of M2-driven inflammatory reactions in vitro and in vivo. p50 NF-kappaB inhibits NF-kappaB-driven, M1-polariz…

LipopolysaccharidesP50Macrophage polarizationRegulatorInflammationBiologyImmune toleranceMiceCell polaritymedicineImmune ToleranceMacrophageAnimalsHumansCells CulturedMice KnockoutMultidisciplinaryMacrophagesCell PolarityNF-kappa B p50 SubunitNF-kappa B p50 SubunitInterferon-betaBiological SciencesCell biologyEndotoxinsSTAT1 Transcription FactorImmunologymedicine.symptom
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Rilpivirine attenuates liver fibrosis through selective STAT1-mediated apoptosis in hepatic stellate cells

2020

ObjectiveLiver fibrosis constitutes a major health problem worldwide due to its rapidly increasing prevalence and the lack of specific and effective treatments. Growing evidence suggests that signalling through cytokine-activated Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathways regulates liver fibrosis and regeneration. Rilpivirine (RPV) is a widely used anti-HIV drug not reported to produce hepatotoxicity. We aimed to describe the potential hepatoprotective effects of RPV in different models of chronic liver injury, focusing on JAK-STAT signalling regulation.DesignThe effects of RPV on hepatic steatosis, inflammation and fibrogenesis were studied in a nut…

Liver CirrhosisSTAT3 Transcription Factor0301 basic medicineApoptosisRisk AssessmentSensitivity and SpecificityMice03 medical and health sciences0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisHepatic Stellate CellsmedicineAnimalsHumansSTAT1610 Medicine & healthSTAT3Cells CulturedLiver injurybiologybusiness.industryRilpivirineFatty liverGastroenterologymedicine.diseaseLiver regenerationLiver RegenerationDisease Models AnimalSTAT1 Transcription FactorTreatment Outcome030104 developmental biology030220 oncology & carcinogenesisbiology.proteinHepatic stellate cellCancer researchbusinessJanus kinase
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Toxoplasma gondii down-regulates MHC class II gene expression and antigen presentation by murine macrophages via interference with nuclear translocat…

2001

The obligate intracellular protozoan parasite Toxoplasma gondii is able to establish persistent infections within human and animal hosts. We have shown recently that T. gondii down-regulates IFN-γ-induced MHC class II expression in murine bone marrow-derived macrophages (BMMΦ). As shown in this study, the capacity of IFN-γ-activated murine BMMΦ to present ovalbumin to CD4+ T cell hybridomas was dose-dependently inhibited by T. gondii. IFN-γ-induced up-regulation of H2-Aa, H2-Ab, H2-Eb, H2-Ma, H2-Mb, H2-Oa and invariant chain transcripts was prominently down-regulated by T. gondii. Furthermore, mRNA levels of class II transactivator and interferon-regulatory factor-1 were significantly dimin…

MHC class IIbiologyT cellImmunologyAntigen presentationToxoplasma gondiibiology.organism_classificationMolecular biologyMHC Class II Genemedicine.anatomical_structureparasitic diseasesbiology.proteinSTAT proteinmedicineImmunology and AllergySTAT1Signal transductionEuropean Journal of Immunology
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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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Partial Sleep Restriction Activates Immune Response-Related Gene Expression Pathways: Experimental and Epidemiological Studies in Humans

2013

Epidemiological studies have shown that short or insufficient sleep is associated with increased risk for metabolic diseases and mortality. To elucidate mechanisms behind this connection, we aimed to identify genes and pathways affected by experimentally induced, partial sleep restriction and to verify their connection to insufficient sleep at population level. The experimental design simulated sleep restriction during a working week: sleep of healthy men (N = 9) was restricted to 4 h/night for five nights. The control subjects (N = 4) spent 8 h/night in bed. Leukocyte RNA expression was analyzed at baseline, after sleep restriction, and after recovery using whole genome microarrays complem…

MaleTBX21NF-KAPPA-Blcsh:MedicineNK cellsBioinformaticskokeellinen tutkimusReceptors G-Protein-Coupled0302 clinical medicineCARDIOMETABOLIC RISKLeukocytesta319geeniekspressiolcsh:Scienceta515Sleep restrictionRegulation of gene expression0303 health sciencesMultidisciplinaryNATURAL-KILLERNF-kappa Bta3142Sleep in non-human animalsC-REACTIVE PROTEIN3. Good healthMACROPHAGE APOPTOSISINSUFFICIENT SLEEPSTAT1 Transcription FactorCARDIOVASCULAR-DISEASEimmuunivasteProteoglycansmedicine.symptomResearch ArticleAdulteducationENDOPLASMIC-RETICULUMMETABOLIC CONSEQUENCESSyntaxin 16Biologyepidemiologinen tutkimusuni (lepotila)03 medical and health sciencesImmune systemmedicineHumans030304 developmental biologyTOLL-LIKE RECEPTORSB cellsuniMicroarray analysis techniquesGene Expression Profilingsytokiinitlcsh:RMicroarray AnalysisGene expression profilingSleep deprivationGene Expression RegulationImmunologyRNASleep Deprivationlcsh:Q3111 BiomedicineT-Box Domain ProteinsReceptors Transforming Growth Factor beta030217 neurology & neurosurgery
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