Search results for "STAT Transcription Factors"

showing 8 items of 8 documents

Interferon-α Suppresses cAMP to Disarm Human Regulatory T Cells

2013

Abstract IFN-α is an antineoplastic agent in the treatment of several solid and hematologic malignancies that exerts strong immune- and autoimmune-stimulating activity. However, the mechanisms of immune activation by IFN-α remain incompletely understood, particularly with regard to CD4+CD25highFoxp+ regulatory T cells (Treg). Here, we show that IFN-α deactivates the suppressive function of human Treg by downregulating their intracellular cAMP level. IFN-α–mediated Treg inactivation increased CD4+ effector T-cell activation and natural killer cell tumor cytotoxicity. Mechanistically, repression of cAMP in Treg was caused by IFN-α–induced MAP–ERK kinase (MEK)/extracellular signal-regulated ki…

MAPK/ERK pathwayCancer Researchmedicine.medical_treatmentGraft vs Host DiseaseAutoimmunitychemical and pharmacologic phenomenaBiologyLymphocyte ActivationT-Lymphocytes RegulatoryNatural killer cellMiceImmune systemDownregulation and upregulationT-Lymphocyte SubsetsCyclic AMPmedicineAnimalsHumansIL-2 receptorPhosphorylationExtracellular Signal-Regulated MAP KinasesCells CulturedMitogen-Activated Protein Kinase KinasesInterleukin-2 Receptor alpha SubunitInterferon-alphaFOXP3hemic and immune systemsDNA-Binding ProteinsKiller Cells NaturalSTAT Transcription Factorsmedicine.anatomical_structureCytokineOncologyHumanized mouseImmunologyCancer researchCancer Research
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The Role of JAK/STAT Molecular Pathway in Vascular Remodeling Associated with Pulmonary Hypertension

2021

Pulmonary hypertension is defined as a group of diseases characterized by a progressive increase in pulmonary vascular resistance (PVR), which leads to right ventricular failure and premature death. There are multiple clinical manifestations that can be grouped into five different types. Pulmonary artery remodeling is a common feature in pulmonary hypertension (PH) characterized by endothelial dysfunction and smooth muscle pulmonary artery cell proliferation. The current treatments for PH are limited to vasodilatory agents that do not stop the progression of the disease. Therefore, there is a need for new agents that inhibit pulmonary artery remodeling targeting the main genetic, molecular,…

0301 basic medicineJanus kinase 2 (JAK2)QH301-705.5Hypertension PulmonaryInflammationReviewVascular Remodeling030204 cardiovascular system & hematologyModels BiologicalCatalysisstatInorganic Chemistry03 medical and health sciences0302 clinical medicinemedicine.arterymedicineAnimalsHumanssignal transducer and activator of transcription 3 (STAT3)pulmonary hypertension (PH)Physical and Theoretical ChemistryEndothelial dysfunctionBiology (General)Molecular BiologyQD1-999SpectroscopyJanus Kinasesbiologybusiness.industryOrganic ChemistryJAK-STAT signaling pathwayGeneral Medicinemedicine.diseasePulmonary hypertensionComputer Science ApplicationsSTAT Transcription FactorsChemistry030104 developmental biologyPulmonary arterybiology.proteinCancer researchmedicine.symptombusinessMyofibroblastPlatelet-derived growth factor receptorSignal TransductionInternational Journal of Molecular Sciences
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Optomotor-blind negatively regulates Drosophila eye development by blocking Jak/STAT signaling

2015

Organ formation requires a delicate balance of positive and negative regulators. In Drosophila eye development, wingless (wg) is expressed at the lateral margins of the eye disc and serves to block retinal development. The T-box gene optomotor-blind (omb) is expressed in a similar pattern and is regulated by Wg. Omb mediates part of Wg activity in blocking eye development. Omb exerts its function primarily by blocking cell proliferation. These effects occur predominantly in the ventral margin. Our results suggest that the primary effect of Omb is the blocking of Jak/STAT signaling by repressing transcription of upd which encodes the Jak receptor ligand Unpaired.

genetic structuresScienceNerve Tissue ProteinsEyeTranscription (biology)ddc:570AnimalsDrosophila ProteinsReceptorTranscription factorCell ProliferationJanus KinasesGeneticsMultidisciplinarybiologyCell growthQRbiology.organism_classificationCell biologySTAT Transcription FactorsDrosophila melanogasterEye developmentMedicineDrosophila melanogasterJanus kinaseT-Box Domain ProteinsDrosophila ProteinResearch ArticleTranscription Factors
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Genome-Wide Inhibition of Pro-atherogenic Gene Expression by Multi-STAT Targeting Compounds as a Novel Treatment Strategy of CVDs.

2018

Cardiovascular diseases (CVDs), including atherosclerosis, are globally the leading cause of death. Key factors contributing to onset and progression of atherosclerosis include the pro-inflammatory cytokines Interferon (IFN)a and IFN? and the Pattern Recognition Receptor (PRR) Toll-like receptor 4 (TLR4). Together, they trigger activation of Signal Transducer and Activator of Transcription (STAT)s. Searches for compounds targeting the pTyr-SH2 interaction area of STAT3, yielded many small molecules, including STATTIC and STX-0119. However, many of these inhibitors do not seem STAT3-specific. We hypothesized that multi-STAT-inhibitors that simultaneously block STAT1, STAT2, and STAT3 activit…

lcsh:Immunologic diseases. Allergy0301 basic medicineMaleIn silicoImmunologyGene ExpressionBiologystatIn silico dockingCell LineSmall Molecule Librariessrc Homology Domains03 medical and health sciencesCVDs treatment strategyImmunology and AllergyAnimalsHumansvascular inflammationSTAT1STAT2STAT3Vascular inflammationCells CulturedOriginal ResearchOxadiazolesGene Expression ProfilingSTATPattern recognition receptorin silico dockingFarmaciaAtherosclerosisCyclic S-OxidesMice Inbred C57BLSTAT Transcription Factors030104 developmental biologyCardiovascular DiseasesTLR4biology.proteinSTAT proteinCancer researchQuinolinesmulti-STAT inhibitorsMulti-STAT inhibitorslcsh:RC581-607Genome-Wide Association StudySignal TransductionFrontiers in immunology
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Oxidative stress inhibits IFN-α-induced antiviral gene expression by blocking the JAK–STAT pathway

2006

Abstract BACKGROUND/AIMS: Unresponsiveness to IFN-alpha is common in chronic hepatitis C. Since conditions associated with an increased oxidative stress (advanced age, steatosis, fibrosis, iron overload, and alcohol consumption) reduce the likelihood of response, we hypothesized that oxidative stress may affect the antiviral actions of IFN-alpha. METHODS: We examined in a human hepatocellular carcinoma cell line (Huh-7) the effect of hydrogen peroxide (H2O2), as a generator of oxidative stress, on the IFN-alpha signaling pathway. RESULTS: Pretreatment of Huh-7 cells with 0.5-1 mM H2O2 resulted in the suppression of the IFN-alpha-induced antiviral protein MxA and of IRF-9 mRNA expression. Th…

Gene Expression Regulation ViralMyxovirus Resistance ProteinsCarcinoma HepatocellularBlotting WesternAntiviral proteinProtein tyrosine phosphataseInterferon alpha-2Biologymedicine.disease_causechemistry.chemical_compoundGTP-Binding ProteinsCell Line TumormedicineHumansRNA NeoplasmHepatologyTyk-2Reverse Transcriptase Polymerase Chain ReactionSTATLiver NeoplasmsInterferon-alphaJAK-STAT signaling pathwayTyrosine phosphorylationHydrogen PeroxideJanus Kinase 1Flow CytometryInterferon-Stimulated Gene Factor 3 gamma SubunitRecombinant ProteinsIFN-aJAK-1Oxidative StressSTAT Transcription FactorsHydrogen peroxide; IFN-a; STAT; JAK-1; Tyk-2chemistryImmunologySTAT proteinCancer researchSignal transductionTyrosine kinaseOxidative stressSignal TransductionJournal of Hepatology
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Differential impact of high and low penetrance TNFRSF1A gene mutations on conventional and regulatory CD4+ T cell functions in TNFR1-associated perio…

2015

Abstract TNFR-associated periodic syndrome is an autoinflammatory disorder caused by autosomal-dominant mutations in TNFRSF1A, the gene encoding for TNFR superfamily 1A. The lack of knowledge in the field of TNFR-associated periodic syndrome biology is clear, particularly in the context of control of immune self-tolerance. We investigated how TNF-α/TNFR superfamily 1A signaling can affect T cell biology, focusing on conventional CD4+CD25− and regulatory CD4+CD25+ T cell functions in patients with TNFR-associated periodic syndrome carrying either high or low penetrance TNFRSF1A mutations. Specifically, we observed that in high penetrance TNFR-associated periodic syndrome, at the molecular le…

Male0301 basic medicinePenetranceAutoimmunitymedicine.disease_causeT-Lymphocytes RegulatoryImmune toleranceSettore MED/38 - Pediatria Generale E SpecialisticaTRAPS; Tconvs; Tregs; autoimmunity; immune toleranceImmunology and AllergyIL-2 receptorChildGeneticsMutationTconvTOR Serine-Threonine Kinaseshemic and immune systemsMiddle AgedAcquired immune systemPenetranceTregSTAT Transcription Factorsmedicine.anatomical_structureReceptors Tumor Necrosis Factor Type ICytokinesFemalebiological phenomena cell phenomena and immunitySignal TransductionAdultAdolescentFeverT cellAutoimmunity; Immune tolerance; Tconvs; Tregs; TRAPS; Cell Biology; ImmunologyImmunologyReceptors Antigen T-CellContext (language use)Tregs[object Object]BiologyImmunophenotypingYoung Adult03 medical and health sciencesImmune systemmedicineHumansAgedCell ProliferationDemographyTconvsImmune toleranceHereditary Autoinflammatory DiseasesTRAPSCell Biologybiological factors030104 developmental biologyMutationCancer research
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Role of JAK/STAT in Interstitial Lung Diseases; Molecular and Cellular Mechanisms

2021

Interstitial lung diseases (ILDs) comprise different fibrotic lung disorders characterized by cellular proliferation, interstitial inflammation, and fibrosis. The JAK/STAT molecular pathway is activated under the interaction of a broad number of profibrotic/pro-inflammatory cytokines, such as IL-6, IL-11, and IL-13, among others, which are increased in different ILDs. Similarly, several growth factors over-expressed in ILDs, such as platelet-derived growth factor (PDGF), transforming growth factor β1 (TGF-β1), and fibroblast growth factor (FGF) activate JAK/STAT by canonical or non-canonical pathways, which indicates a predominant role of JAK/STAT in ILDs. Between the different JAK/STAT iso…

QH301-705.5medicine.medical_treatmentReviewCatalysisstatInorganic ChemistryPulmonary fibrosismedicineHumansProtein IsoformsPhysical and Theoretical ChemistryBiology (General)STAT3Molecular BiologyProtein Kinase InhibitorsQD1-999SpectroscopyCellular SenescenceJanus KinasesbiologyChemistryGrowth factorInterleukinsinterstitial lung disease (ILD)Organic ChemistryJAK-STAT signaling pathwayGeneral Medicinerespiratory systemmedicine.diseaseEndoplasmic Reticulum StressComputer Science Applicationsrespiratory tract diseasesSTAT Transcription FactorsChemistrysignal transducer and activator of transcription (STAT)biology.proteinCancer researchidiopathic pulmonary fibrosis (IPF)Janus kinaseLung Diseases InterstitialJanus kinases (JAK)Platelet-derived growth factor receptorTransforming growth factorSignal TransductionInternational Journal of Molecular Sciences
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Comprehensive estimation of input signals and dynamics in biochemical reaction networks

2012

Abstract Motivation: Cellular information processing can be described mathematically using differential equations. Often, external stimulation of cells by compounds such as drugs or hormones leading to activation has to be considered. Mathematically, the stimulus is represented by a time-dependent input function. Parameters such as rate constants of the molecular interactions are often unknown and need to be estimated from experimental data, e.g. by maximum likelihood estimation. For this purpose, the input function has to be defined for all times of the integration interval. This is usually achieved by approximating the input by interpolation or smoothing of the measured data. This procedu…

Statistics and ProbabilityMedicin och hälsovetenskapComputer scienceDifferential equationMaximum likelihoodcomputer.software_genreBiochemistryModels BiologicalMedical and Health SciencesIntegration intervalMolecular BiologyJanus KinasesLikelihood FunctionsRegulation Pathways and Systems BiologyExperimental dataOriginal PapersConfidence intervalComputer Science ApplicationsComputational MathematicsSTAT Transcription FactorsComputational Theory and MathematicsData miningAlgorithmcomputerSmoothingAlgorithmsSignal Transduction
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