Search results for "Trans-Activator"

showing 10 items of 113 documents

Asthmatic changes in mice lacking T-bet are mediated by IL-13

2005

Mice with a targeted deletion of the T-bet gene exhibit spontaneous airway hyperresponsiveness (AHR), airway inflammation, enhanced recovery of T(h)2 cytokines from bronchoalveolar lavage fluid, sub-epithelial collagen deposition and myofibroblast transformation. Here we analyze the mechanisms responsible for the chronic airway remodeling observed in these mice. CD4+ T cells isolated from the lung of T-bet-deficient mice were spontaneously activated CD44(high)CD69(high) memory T cells, with a typical T(h)2 cytokine profile. Neutralization of IL-13 but not IL-4 resulted in amelioration of AHR in airways of mice lacking T-bet. IL-13 blockade also led to reduced eosinophilia and decreased vime…

CD4-Positive T-LymphocytesImmunologychemical and pharmacologic phenomenaVimentinLymphocyte ActivationSmad7 ProteinMiceTransforming Growth Factor betamedicineAnimalsVimentinImmunology and AllergyEosinophiliaSmad3 ProteinLungCells CulturedMice KnockoutInterleukin-13Lungbiologymedicine.diagnostic_testChemistryCD69hemic and immune systemsGeneral MedicineTransforming growth factor betaFibroblastsrespiratory systemActinsAsthmarespiratory tract diseasesDNA-Binding ProteinsMice Inbred C57BLBronchoalveolar lavagemedicine.anatomical_structureInterleukin 13ImmunologyTrans-Activatorsbiology.proteinCytokinesInterleukin-4medicine.symptomT-Box Domain ProteinsImmunologic MemoryMyofibroblastTranscription FactorsInternational Immunology
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The receptor NLRP3 is a transcriptional regulator of TH2 differentiation.

2015

The receptor NLRP3 is involved in the formation of the NLRP3 inflammasome that activates caspase-1 and mediates the release of interleukin 1β (IL-1β) and IL-18. Whether NLRP3 can shape immunological function independently of inflammasomes is unclear. We found that NLRP3 expression in CD4(+) T cells specifically supported a T helper type 2 (TH2) transcriptional program in a cell-intrinsic manner. NLRP3, but not the inflammasome adaptor ASC or caspase-1, positively regulated a TH2 program. In TH2 cells, NLRP3 bound the Il4 promoter and transactivated it in conjunction with the transcription factor IRF4. Nlrp3-deficient TH2 cells supported melanoma tumor growth in an IL-4-dependent manner and …

CD4-Positive T-LymphocytesInflammasomesImmunologyBlotting WesternBiologyInterleukin 21MiceTh2 CellsCell Line TumorNLR Family Pyrin Domain-Containing 3 ProteinImmunology and AllergyCytotoxic T cellAnimalsIL-2 receptorPromoter Regions GeneticInterleukin 3Oligonucleotide Array Sequence AnalysisMice KnockoutCD40integumentary systemReverse Transcriptase Polymerase Chain ReactionZAP70Gene Expression ProfilingCell DifferentiationNeoplasms ExperimentalAsthmaCell biologyGene Expression Regulation NeoplasticMice Inbred C57BLInterleukin 10Interferon Regulatory FactorsInterleukin 12biology.proteinNIH 3T3 CellsTrans-ActivatorsFemaleInterleukin-4Carrier ProteinsProtein BindingSignal TransductionNature immunology
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A new model of chronic colitis in SCID mice induced by adoptive transfer of CD62L+ CD4+ T cells: insights into the regulatory role of interleukin-6 o…

2003

<i>Objective:</i> The proinflammatory cytokine interleukin (IL)-6 is involved in various chronic inflammatory processes. IL-6 is a predominant cytokine produced by lamina propria T cells in Crohn’s disease and experimental colitis. This study was designed to examine the effect of a neutralizing IL-6-receptor (IL-6R) antibody on the programmed cell death of mucosal T cells in the CD62L+ CD4+ SCID transfer model of chronic experimental colitis in mice and to gain more insight into the pathogenesis of this transfer colitis model. <i>Methods:</i> For adoptive transfer, we isolated CD62L+ CD4+ double-positive T cells from wild-type BALB/c mice followed by intraperitoneal …

CD4-Positive T-LymphocytesSTAT3 Transcription FactorAdoptive cell transferCell TransplantationColonApoptosisMice SCIDPathology and Forensic MedicineProinflammatory cytokineInterleukin 21MiceInterleukin 25In Situ Nick-End LabelingAnimalsIL-2 receptorIntestinal MucosaL-SelectinInterleukin 6Antibodies BlockingMolecular BiologyMice Inbred BALB CbiologyInterleukin-6InterleukinCell BiologyGeneral MedicineFlow CytometryAdoptive TransferReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalImmunologybiology.proteinTrans-ActivatorsInterleukin 18Colitis UlcerativeSevere Combined ImmunodeficiencySpleenPathobiology : journal of immunopathology, molecular and cellular biology
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Activation pattern of signal transducers and activators of transcription (STAT) factors in inflammatory bowel diseases.

2005

Cytokine signaling pathways involving transcription factors of the signal transducers and activators of transcription (STAT) family play a key role in the pathogenesis of inflammatory bowel diseases (IBD). STAT proteins are latent cytoplasmic transcription factors that induce transcription upon phosphorylation, dimerization, and nuclear translocation. However, their activation pattern in IBD is poorly understood. The aim of our study was to characterize STAT-expression in IBD.Mononuclear cells were isolated from 36 colonic specimens of Crohn's disease, ulcerative colitis, or from control patients. Cells were stimulated overnight with antibodies against human CD2 and CD28 and mononuclear cel…

CD4-Positive T-LymphocytesSTAT3 Transcription FactorColonActivation patternstatTranscription (biology)MedicineHumansSTAT4Transcription factorHepatologybusiness.industryActivator (genetics)digestive oral and skin physiologyGastroenterologySTAT2 Transcription FactorSTAT3 Transcription FactorSTAT4 Transcription FactorInflammatory Bowel Diseasesdigestive system diseasesDNA-Binding ProteinsSTAT1 Transcription FactorCase-Control StudiesImmunologyCancer researchTrans-ActivatorsSignal transductionbusinessSTAT6 Transcription FactorThe American journal of gastroenterology
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H2-M, a facilitator of MHC class II peptide loading, and its negative modulator H2-O are differentially expressed in response to proinflammatory cyto…

2000

H2-M is a major histocompatibility complex (MHC) class II-like molecule that catalyzes peptide binding to MHC class II molecules. Recently, the H2-O heterodimer, encoded by H2-Oa and H2-Ob in the MHC class II region, has been shown to be physically associated with H2-M in B cells and to downregulate H2-M function. Examination of H2-O expression in freshly isolated mouse organs revealed that H2-Oa- and H2-Ob-specific transcripts are present in both lymphoid and nonlymphoid tissues. To evaluate the gene regulation and functional impact of H2-O on antigen presentation, we examined the effects on MHCII, invariant chain (Ii), H2-M, and H2-O gene expression of interleukin (IL)-4, IL-10, and inter…

CD74ImmunologyAntigen presentationchemical and pharmacologic phenomenaMajor histocompatibility complexInterferon-gammaMiceMHC class IGeneticsCIITAAnimalsTissue DistributionRNA MessengerAntigen PresentationHLA-D AntigensMHC class IIbiologyAntigen processingHistocompatibility Antigens Class IINuclear ProteinsMHC restrictionMolecular biologyInterleukin-10Antigens Differentiation B-LymphocyteGene Expression RegulationMice Inbred DBATrans-Activatorsbiology.proteinInterleukin-4PeptidesImmunogenetics
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Downregulation of wild-type β-catenin expression by interleukin 6 in human hepatocarcinoma HepG2 cells: a possible role in the growth-regulatory effe…

2001

We investigated the antitumour effects of interleukin 6 (IL-6) on hepatocarcinoma HepG2 cells, endowed with high levels of a mutated, non-degradable, beta-catenin. IL-6 produced minimal growth-inhibitory effects and no apoptosis or gross changes in cell adhesion. Interestingly, however, it caused a consistent decrease in the cytoplasmic levels of wild-type, but not of mutated, beta-catenin protein. There was no effect on E-cadherin or gamma-catenin and a reduction in alpha-catenin occurred only at high concentrations. IL-4, a non-related cytokine, did not modify the content of beta-catenin. IL-6 did not influence beta-catenin mRNA levels. LiCl, a potent inhibitor of Glycogen Synthase Kinase…

Cancer ResearchCarcinoma Hepatocellularmedicine.medical_treatmentBlotting WesternDown-RegulationApoptosisEnzyme-Linked Immunosorbent AssayBiologyDownregulation and upregulationGSK-3Tumor Cells CulturedmedicineHumansRNA MessengerInterleukin 6beta CateninInterleukin 4Interleukin-6Cell growthLiver NeoplasmsWild typeCell biologyCytoskeletal ProteinsCytokineOncologyCateninTrans-ActivatorsCancer researchbiology.proteinEuropean Journal of Cancer
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Dual regulation of SPI1/PU.1 transcription factor by heat shock factor 1 (HSF1) during macrophage differentiation of monocytes

2014

International audience; : In addition to their cytoprotective role in stressful conditions, heat shock proteins (HSPs) are involved in specific differentiation pathways, e.g. we have identified a role for HSP90 in macrophage differentiation of human peripheral blood monocytes exposed to Macrophage Colony-Stimulating Factor (M-CSF). Here, we show that deletion of the main transcription factor involved in heat shock gene regulation, heat shock factor 1 (HSF1), affects M-CSF-driven differentiation of mouse bone marrow cells. HSF1 transiently accumulates in the nucleus of human monocytes undergoing macrophage differentiation, including M-CSF-treated peripheral blood monocytes and phorbol ester-…

Cancer ResearchCellular differentiation[SDV]Life Sciences [q-bio][SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]Mice0302 clinical medicineHeat Shock Transcription FactorsHSF1[SDV.BDD]Life Sciences [q-bio]/Development BiologyCells CulturedComputingMilieux_MISCELLANEOUSRegulation of gene expression0303 health sciencesMice Inbred BALB C[SDV.MHEP.HEM]Life Sciences [q-bio]/Human health and pathology/HematologyHematology[SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry Molecular Biology/Biomolecules [q-bio.BM]3. Good healthDNA-Binding ProteinsOncology030220 oncology & carcinogenesismonocytesProteasome Endopeptidase ComplexAntigens Differentiation MyelomonocyticReceptors Cell Surface[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiology03 medical and health sciencesAntigens CDHeat shock proteinProto-Oncogene Proteinstranscription factorsAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biology[ SDV.BDD ] Life Sciences [q-bio]/Development BiologyTranscription factor030304 developmental biologySPI1Macrophagesheat-shock proteinsfungi[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyMolecular biologyHsp70Heat shock factorMice Inbred C57BLcell differentiationGene Expression RegulationTrans-Activators[SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
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Regulation of human inducible nitric oxide synthase expression by an upstream open reading frame.

2019

Abstract The human inducible nitric oxide synthase (iNOS) gene contains an upstream open reading frame (uORF) in its 5′-untranslated region (5′-UTR) implying a translational regulation of iNOS expression. Transfection experiments in human DLD-1 cells revealed that the uORF although translatable seems not to inhibit the translation start at the bona fide ATG. Our data clearly show that human iNOS translation is cap-dependent and that the 5′-UTR of the iNOS mRNA contains no internal ribosome entry site. Translation of the bona fide coding sequence is most likely mediated by a leaky scanning mechanism. The 5′-UTR is encoded by exon 1 and exon 2 of the iNOS gene with the uORF stop codon located…

Cancer ResearchFive prime untranslated regionPhysiologyClinical BiochemistryDown-RegulationNitric Oxide Synthase Type IILeaky scanningBiochemistryExonOpen Reading FramesCell Line TumorUpstream open reading frameTranslational regulationCoding regionHumansAmino Acid SequenceBase SequenceChemistryIntronExonsIntronsCell biologyNonsense Mediated mRNA DecayInternal ribosome entry siteGene Expression RegulationMutationTrans-ActivatorsRNA HelicasesNitric oxide : biology and chemistry
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Breast cancer genome-wide association studies: there is strength in numbers.

2012

Breast cancer (BC) is a heterogeneous disease that exhibits familial aggregation. Family linkage studies have identified high-penetrance genes, BRCA1, BRCA2, PTEN and TP53, that are responsible for inherited BC syndromes. Moreover, a combination of family-based and population-based approaches indicated that genes involved in DNA repair, such as CHEK2, ATM, BRIP and PALB2, are associated with moderate risk. Therefore, all of these known genes account for only 25% of the familial aggregation cases. Recently, genome wide association studies (GWAS) in BC revealed single nucleotide polymorphisms (SNPs) in five novel genes associated to susceptibility: TNRC9, FGFR2, MAP3K1, H19 and lymphocyte-spe…

Cancer ResearchMultifactorial InheritanceSettore MED/06 - Oncologia MedicaPALB2PopulationMAP Kinase Kinase Kinase 1Single-nucleotide polymorphismGenome-wide association studyBreast NeoplasmsBiologyPolymorphism Single NucleotideGenetic linkageGeneticsSNPHumansGenetic Predisposition to DiseaseReceptor Fibroblast Growth Factor Type 2educationMolecular BiologyGeneCHEK2Geneticsbreast cancer GWASeducation.field_of_studyMicrofilament ProteinsHigh Mobility Group ProteinsCancer researchTrans-ActivatorsFemaleApoptosis Regulatory ProteinsReceptors ProgesteroneGenome-Wide Association StudyOncogene
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EWS/FLI-1 rearrangement in small round cell sarcomas of bone and soft tissue detected by reverse transcriptase polymerase chain reaction amplificatio…

1994

Recent cloning of the t(11;22) region has led to the detection of a number of sequences involved in the breakpoints by substituting a sequence which encodes a putative RNA binding domain for that of the DNA binding domain of the human homologue of murine FLI-1. Several tumours display consistent translocation at t(11;22) (q24;q12), a finding that suggests these fusion transcripts could be expressed and detected by reverse transcriptase polymerase chain reaction amplification. To date, only a small number of Ewing's sarcomas (Es) and peripheral neuroectodermal tumours (pPNET) of bone have been tested with this novel molecular biology approach. In this study, we confirmed the presence of the …

Cancer ResearchPathologymedicine.medical_specialtyChromosomes Human Pair 22Molecular Sequence DataTransplantation HeterologousEctomesenchymomaMice NudeBone NeoplasmsSoft Tissue NeoplasmsSarcoma EwingBone SarcomaBiologyPolymerase Chain ReactionTranslocation GeneticMiceProto-Oncogene ProteinsmedicineAnimalsHumansNeuroectodermal tumorBase SequenceProto-Oncogene Protein c-fli-1Soft tissue sarcomaChromosomes Human Pair 11Ewing's sarcomaRNA-Directed DNA PolymeraseGene rearrangementmedicine.diseaseDNA-Binding ProteinsReal-time polymerase chain reactionOncologySarcoma Small CellCancer researchTrans-ActivatorsOsteosarcomaEuropean journal of cancer (Oxford, England : 1990)
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