Search results for "MICE"

showing 10 items of 6027 documents

Differential Regulation of CCL22 Gene Expression in Murine Dendritic Cells and B Cells

2005

Abstract The activated T cell-attracting CC chemokine CCL22 is expressed by stimulated B cells and mature dendritic cells (DC). We have cloned and sequenced the complete mouse gene, including 4 kb of the 5′-flanking promoter region, and detected two distinct sites for initiation of transcription by 5′-RACE. Reporter gene assays indicate that the promoter reflects the specificity of the endogenous gene. Within the proximal promoter region, we identified potential binding sites for NF-κB, Ikaros, and a putative GC box. All three regions bind proteins. The NF-κB site was shown to specifically bind NF-κB subunits p50 and p65 from nuclear extracts of LPS-stimulated B cells, B cell line A20/2J, T…

Transcriptional ActivationSp1 Transcription FactorMolecular Sequence DataImmunologyCAAT boxBiologyCell LineMiceTransactivationGene expressionAnimalsImmunology and AllergyCloning MolecularProtein PrecursorsBinding sitePromoter Regions GeneticGeneChemokine CCL22B-LymphocytesMice Inbred BALB CReporter geneBinding SitesBinding proteinNF-kappa BTranscription Factor RelANF-kappa B p50 SubunitPromoterDendritic CellsMolecular biologyDNA-Binding ProteinsMice Inbred C57BLGene Expression RegulationChemokines CCMutagenesis Site-DirectedNIH 3T3 CellsFemaleTranscription Initiation SiteThe Journal of Immunology
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TGFβ-induced EMT requires focal adhesion kinase (FAK) signaling

2007

The epithelial-to-mesenchymal transition (EMT) is a crucial process, occurring both during development and tumor progression, by which an epithelial cell undergoes a conversion to a mesenchymal phenotype, dissociates from initial contacts and migrates to secondary sites. We recently reported that in hepatocytes the multifunctional cytokine TGFβ induces a full EMT characterized by (i) Snail induction, (ii) E-cadherin delocalization and down-regulation, (iii) down-regulation of the hepatocyte transcriptional factor HNF4α and (iv) up-regulation of mesenchymal and invasiveness markers. In particular, we showed that Snail directly causes the transcriptional down-regulation of E-cadherin and HN…

Transcriptional ActivationTGFβFAK; MT; Src; TGFβ; Animals; Biomarkers Tumor; Cadherins; Cell Line; Cell Transformation Neoplastic; Enzyme Activation; Epithelial Cells; Focal Adhesion Protein-Tyrosine Kinases; Hepatocytes; Liver Neoplasms; Mesoderm; Mice; Neoplasm Invasiveness; Signal Transduction; Transcriptional Activation; Transforming Growth Factor beta; Up-Regulation; src-Family Kinases; Cell BiologyCell LineMesodermFocal adhesionMiceTransforming Growth Factor betaBiomarkers TumorAnimalsHepatocyteNeoplasm InvasivenessNeoplasm InvasiveneEpithelial CellFocal Adhesion Protein-Tyrosine KinaseFAKbiologyAnimalCadherinLiver NeoplasmsMesenchymal stem cellEpithelial CellsCell BiologyTransforming growth factor betaTgf beta; fak; srcCadherinsUp-RegulationCell biologyEnzyme ActivationCell Transformation Neoplasticsrc-Family KinasesHepatocyte nuclear factor 4Liver NeoplasmTumor progressionMTFocal Adhesion Protein-Tyrosine KinasesCadherinHepatocytesCancer researchbiology.proteinsrc-Family KinaseSignal transductionSrcSignal TransductionProto-oncogene tyrosine-protein kinase SrcExperimental Cell Research
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The Wilms' tumor suppressor gene (wt1) product regulates Dax-1 gene expression during gonadal differentiation.

1999

Gonadal differentiation is dependent upon a molecular cascade responsible for ovarian or testicular development from the bipotential gonadal ridge. Genetic analysis has implicated a number of gene products essential for this process, which include Sry, WT1, SF-1, and DAX-1. We have sought to better define the role of WT1 in this process by identifying downstream targets of WT1 during normal gonadal development. We have noticed that in the developing murine gonadal ridge, wt1 expression precedes expression of Dax-1, a nuclear receptor gene. We document here that the spatial distribution profiles of both proteins in the developing gonad overlap. We also demonstrate that WT1 can activate the D…

Transcriptional Activationcongenital hereditary and neonatal diseases and abnormalitiesGenes Wilms TumorReceptors Retinoic AcidTATA boxMolecular Sequence DataMutagenesis (molecular biology technique)Biologyurologic and male genital diseasesResponse ElementsTransactivationMiceGene expressionAnimalsHumansGonadsPromoter Regions GeneticWT1 ProteinsMolecular BiologyGeneCell Growth and DevelopmentCell Line TransformedGonadal ridgeBase Sequenceurogenital systemDAX-1 Orphan Nuclear ReceptorfungiGene Expression Regulation DevelopmentalCell Biologyfemale genital diseases and pregnancy complicationsCell biologyDNA-Binding ProteinsRepressor ProteinsTestis determining factorNuclear receptorCOS CellsCancer researchTranscription FactorsMolecular and cellular biology
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Physiological activation of the IgH 3' enhancer in B lineage cells is not blocked by Pax-5.

1996

The mouse 3' enhancer contains a high-affinity binding site for the paired box protein Pax-5. Here, we demonstrate by genomic footprinting that the rat 3' enhancer contains a low-affinity binding site for Pax-5, which is occupied in activated splenic B cells. Thus, binding of Pax-5 to the IgH 3' enhancer appears to be evolutionarily conserved in rodents. Analysis of Pax-5 expression in primary B cells demonstrates that Pax-5 remains expressed after 4 days of lipopolysaccharide (LPS) induction, but is down-regulated in 5-day stimulated cells. Similarly, the expression of Pax-5 is down-regulated in vivo in activated large splenocytes, in contrast to small resting cells. Multimerization of the…

Transcriptional Activationcongenital hereditary and neonatal diseases and abnormalitiesanimal structuresImmunologyCD40 LigandDNA FootprintingHeterologousDown-RegulationReceptors Antigen B-CellEnhancer RNAsLymphocyte ActivationMiceGene expressionImmunology and AllergyAnimalsBinding siteEnhancerTranscription factorCells CulturedReporter geneB-LymphocytesCD40Membrane GlycoproteinsbiologyGenes ImmunoglobulinPAX5 Transcription FactorNuclear ProteinsMolecular biologyRatsUp-Regulationbody regionsDNA-Binding ProteinsRepressor ProteinsEnhancer Elements GeneticGene Expression Regulationembryonic structuresbiology.proteinTrans-Activatorssense organsTranscription FactorsEuropean journal of immunology
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Release of dendritic cells from cognate CD4 + T-cell recognition results in impaired peripheral tolerance and fatal cytotoxic T-cell mediated autoimm…

2012

Resting dendritic cells (DCs) induce tolerance of peripheral T cells that have escaped thymic negative selection and thus contribute significantly to protection against autoimmunity. We recently showed that CD4 + Foxp3 + regulatory T cells (Tregs) are important for maintaining the steady-state phenotype of DCs and their tolerizing capacity in vivo. We now provide evidence that DC activation in the absence of Tregs is a direct consequence of missing DC–Treg interactions rather than being secondary to generalized autoimmunity in Treg-less mice. We show that DCs that lack MHC class II and thus cannot make cognate interactions with CD4 + T cells are completely unable to induce peripheral CD8 +…

TransgeneGenes MHC Class IIAutoimmunityMice Transgenicchemical and pharmacologic phenomenaAdaptive ImmunityLymphocyte Activationmedicine.disease_causeT-Lymphocytes RegulatoryAutoimmunityMicemedicineAnimalsCytotoxic T cellHomeodomain ProteinsMHC class IIMultidisciplinarybiologyPeripheral ToleranceBody WeightHistological TechniquesFOXP3Peripheral tolerancehemic and immune systemsDendritic CellsBiological SciencesFlow CytometryAcquired immune systemTamoxifenImmunologybiology.proteinCD8T-Lymphocytes CytotoxicProceedings of the National Academy of Sciences
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Development of S/MAR minicircles for enhanced and persistent transgene expression in the mouse liver.

2010

We have previously described the development of a scaffold/matrix attachment region (S/MAR) episomal vector system for in vivo application and demonstrated its utility to sustain transgene expression in the mouse liver for at least 6 months following a single administration. Subsequently, we observed that transgene expression is sustained for the lifetime of the animal. The level of expression, however, does drop appreciably over time. We hypothesised that by eliminating the bacterial components in our vectors, we could improve their performance since bacterial sequences have been shown to be responsible for the immunotoxicity of the vector and the silencing of its expression when applied i…

TransgeneGenetic VectorsEnzyme-Linked Immunosorbent AssayBiologyMinicircleMolecular biologyPolymerase Chain ReactionScaffold/matrix attachment region (S/MAR) – Minicircle – Plasmid – Non-viral – Gene therapy – Liver – Hydrodynamic deliveryBlotting SouthernMicePlasmidSettore MED/38 - Pediatria Generale E SpecialisticaLiverIn vivoCell Line TumorDrug DiscoveryGene expressionMolecular MedicineGene silencingAnimalsHumansExpression cassetteTransgenesScaffold/matrix attachment regionGenetics (clinical)Journal of molecular medicine (Berlin, Germany)
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Hydrodynamic liver gene transfer mechanism involves transient sinusoidal blood stasis and massive hepatocyte endocytic vesicles

2005

The present study contributes to clarify the mechanism underlying the high efficacy of hepatocyte gene transfer mediated by hydrodynamic injection. Gene transfer experiments were performed employing the hAAT gene, and the efficacy and differential identification in mouse plasma of human transgene versus mouse gene was assessed by ELISA and proteomic procedures, respectively. By applying different experimental strategies such as cumulative dose-response efficacy, hemodynamic changes reflected by venous pressures, intravital microscopy, and morphological changes established by transmission electron microscopy, we found that: (a) cumulative multiple doses of transgene by hydrodynamic injection…

TransgeneGenetic VectorsMolecular Sequence DataEnzyme-Linked Immunosorbent AssayVena Cava InferiorBlood stasisGene deliveryBiologyMiceGeneticsmedicineAnimalsHumansMolecular BiologyPortal VeinCytoplasmic VesiclesGenetic transferGene Transfer TechniquesBlood flowMolecular biologyEndocytosisCell biologyMice Inbred C57BLMicroscopy ElectronEndocytic vesiclemedicine.anatomical_structurealpha 1-AntitrypsinHepatocyteHepatocytesMolecular MedicineVenous PressureIntravital microscopyLiver CirculationGene Therapy
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Dendritic cell-derived IL-12p40 homodimer contributes to susceptibility in cutaneous leishmaniasis in BALB/c mice

2007

Abstract Protection against Leishmania major in resistant C57BL/6 mice is mediated by Th1 cells, whereas susceptibility in BALB/c mice is the result of Th2 development. IL-12 release by L. major-infected dendritic cells (DC) is critically involved in differentiation of Th1 cells. Previously, we reported that strain differences in the production of DC-derived factors, e.g., IL-1αβ, are in part responsible for disparate disease outcome. In the present study, we analyzed the release of IL-12 from DC in more detail. Stimulated DC from C57BL/6 and BALB/c mice released comparable amounts of IL-12p40 and p70. In the absence of IL-4, BALB/c DC produced significantly more IL-12p40 than C57BL/6 DC. D…

TransgeneImmunologyLeishmaniasis CutaneousMice TransgenicBiologyBALB/cMiceWestern blotSpecies SpecificityIn vivoImmunitymedicineImmunology and AllergyAnimalsLeishmania majorGenetic Predisposition to DiseaseCells CulturedLeishmania majorMice Inbred BALB Cmedicine.diagnostic_testInterleukin-12 Subunit p40Dendritic cellDendritic Cellsbiology.organism_classificationMolecular biologyInterleukin-12In vitroImmunity InnateMice Inbred C57BLImmunologyInterleukin-4DimerizationSignal Transduction
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Differential Roles of Macrophages in Diverse Phases of Skin Repair

2010

Abstract Influx of macrophages plays a crucial role in tissue repair. However, the precise function of macrophages during the healing response has remained a subject of debate due to their functional dichotomy as effectors of both tissue injury and repair. We tested the hypothesis that macrophages recruited during the diverse phases of skin repair after mechanical injury exert specific functions to restore tissue integrity. For this purpose, we developed a mouse model that allows conditional depletion of macrophages during the sequential stages of the repair response. Depletion of macrophages restricted to the early stage of the repair response (inflammatory phase) significantly reduced the…

TransgeneImmunologyMice TransgenicCell SeparationBiologyFlow cytometryMiceSkin Physiological PhenomenamedicineAnimalsImmunology and AllergySkinSkin repairWound HealingSkin Physiological Phenomenamedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionEffectorMacrophagesGranulation tissueFlow CytometryImmunohistochemistryCell biologyMice Inbred C57BLmedicine.anatomical_structureImmunologyImmunohistochemistryFunction (biology)The Journal of Immunology
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Regulatory T Cells More Effectively Suppress Th1-Induced Airway Inflammation Compared with Th2

2011

Abstract Asthma is a syndrome with different inflammatory phenotypes. Animal models have shown that, after sensitization and allergen challenge, Th2 and Th1 cells contribute to the development of allergic airway disease. We have previously demonstrated that naturally occurring regulatory T cells (nTregs) can only marginally suppress Th2-induced airway inflammation and airway hyperresponsiveness. In this study, we investigated nTreg-mediated suppression of Th2-induced and Th1-induced acute allergic airway disease. We demonstrate in vivo that nTregs exert their suppressive potency via cAMP transfer on Th2- and Th1-induced airway disease. A comparison of both phenotypes revealed that, despite …

TransgeneImmunologyMice TransgenicInflammationT-Lymphocytes RegulatoryMiceTh2 CellsIn vivoImmunitymedicineAnimalsImmunology and AllergyPotencyCells CulturedSensitizationAsthmaInflammationMice KnockoutMice Inbred BALB Cbusiness.industryTh1 Cellsrespiratory systemmedicine.diseasePhenotypeCoculture TechniquesImmunity Innaterespiratory tract diseasesDisease Models Animalmedicine.anatomical_structureAcute DiseaseImmunologyFemaleDisease SusceptibilityBronchial Hyperreactivitymedicine.symptombusinessThe Journal of Immunology
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