Search results for "script"

showing 10 items of 5143 documents

Overexpression of bone morphogenetic protein-6 (BMP-6) in murine epidermis suppresses skin tumor formation by induction of apoptosis and downregulati…

2001

Bone morphogenetic protein-6 (BMP-6) is a member of the transforming growth factor-beta superfamily. In murine skin, BMP-6 is highly expressed in postmitotic keratinocytes from day 15.5 p.c. till day 6 p.p. Expression in adult skin remains at very low levels, but pathological conditions such as wounding induce the expression of BMP-6. We demonstrate that tumor promotion by TPA (12-O-tetradecanoylphorbol-13-acetate) also induces expression of BMP-6 in suprabasal keratinocytes. This induction is due to post-transcriptional regulation since the level of BMP-6 mRNA remained unchanged. We performed two-stage skin carcinogenesis experiments with transgenic mice epidermally overexpressing BMP-6. T…

Genetically modified mouseKeratinocytesCancer ResearchSkin NeoplasmsBone Morphogenetic Protein 6Transgene910-Dimethyl-12-benzanthraceneDown-RegulationApoptosisMice TransgenicBiologymedicine.disease_causeMiceDownregulation and upregulationGenes junGeneticsmedicineIn Situ Nick-End LabelingTumor Cells CulturedAnimalsRNA MessengerMolecular BiologyIn Situ Hybridizationintegumentary systemActivator (genetics)Reverse Transcriptase Polymerase Chain ReactionGenes fosImmunohistochemistryCell biologyBone morphogenetic protein 6ApoptosisImmunologyBone Morphogenetic ProteinsMutationTetradecanoylphorbol AcetateTumor promotionEpidermisCarcinogenesisCell DivisionOncogene
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TGF-beta1 in liver fibrosis: an inducible transgenic mouse model to study liver fibrogenesis.

1999

Transforming growth factor-beta1 (TGF-beta1) is a powerful stimulus for collagen formation in vitro. To determine the in vivo effects of TGF-beta1 on liver fibrogenesis, we generated transgenic mice overexpressing a fusion gene [C-reactive protein (CRP)/TGF-beta1] consisting of the cDNA coding for an activated form of TGF-beta1 under the control of the regulatory elements of the inducible human CRP gene promoter. Two transgenic lines were generated with liver-specific overexpression of mature TGF-beta1. After induction of the acute phase response (15 h) with lipopolysaccharide (100 microgram ip), plasma TGF-beta1 levels reached600 ng/ml in transgenic animals, which is100 times above normal …

Genetically modified mouseLipopolysaccharidesmedicine.medical_specialtyTranscription GeneticPhysiologyTransgeneRecombinant Fusion ProteinsMice TransgenicBiologyRegulatory Sequences Nucleic AcidLiver Cirrhosis ExperimentalMiceDownregulation and upregulationFibrosisIn vivoTransforming Growth Factor betaPhysiology (medical)Internal medicinemedicineAnimalsHumansRNA MessengerPromoter Regions GeneticRegulation of gene expressionHepatologyGastroenterologymedicine.diseaseMolecular biologyImmunohistochemistryEndocrinologymedicine.anatomical_structureC-Reactive ProteinGene Expression RegulationLiverHepatocyteHepatic stellate cellCollagenProcollagen
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Treatment of allergic airway inflammation and hyperresponsiveness by antisense-induced local blockade of GATA-3 expression.

2001

Recent studies in transgenic mice have revealed that expression of a dominant negative form of the transcription factor GATA-3 in T cells can prevent T helper cell type 2 (Th2)-mediated allergic airway inflammation in mice. However, it remains unclear whether GATA-3 plays a role in the effector phase of allergic airway inflammation and whether antagonizing the expression and/or function of GATA-3 can be used for the therapy of allergic airway inflammation and hyperresponsiveness. Here, we analyzed the effects of locally antagonizing GATA-3 function in a murine model of asthma. We could suppress GATA-3 expression in interleukin (IL)-4–producing T cells in vitro and in vivo by an antisense ph…

Genetically modified mouseOvalbuminmedicine.medical_treatmentImmunologyT cellsInflammationGATA3 Transcription FactorGATA-3Proinflammatory cytokineMiceTh2 CellsImmunology and AllergyMedicineAnimalsInterleukin 9LungInterleukin 4Mice Inbred BALB Cbiologybusiness.industryInterleukin-9InterleukinOligonucleotides Antisenseasthmaantisense DNADNA-Binding ProteinsEosinophilsOvalbuminCytokineImmunologybiology.proteinTrans-ActivatorsFemaleOriginal ArticleInterleukin-4Th2 cytokinesmedicine.symptomBronchial HyperreactivitybusinessThe Journal of experimental medicine
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TGF-β Suppresses Tumor Progression in Colon Cancer by Inhibition of IL-6 trans-Signaling

2004

Alterations of TGF-beta signaling have been described in colorectal cancer, although the molecular consequences are largely unknown. By using transgenic mice overexpressing TGF-beta or a dominant-negative TGF-betaRII, we demonstrate that TGF-beta signaling in tumor infiltrating T lymphocytes controls the growth of dysplastic epithelial cells in experimental colorectal cancer, as determined by histology and a novel system for high-resolution chromoendoscopy. At the molecular level, TGF-beta signaling in T cells regulated STAT-3 activation in tumor cells via IL-6. IL-6 signaling required tumor cell-derived soluble IL-6R rather than membrane bound IL-6R and suppression of such TGF-beta-depende…

Genetically modified mouseSTAT3 Transcription FactorColorectal cancerRecombinant Fusion ProteinsT-LymphocytesImmunologyBlotting WesternEnzyme-Linked Immunosorbent AssayMice TransgenicProtein Serine-Threonine KinasesMiceIn vivoTransforming Growth Factor betamedicineImmunology and AllergyAnimalsHumansEndoscopy Digestive SystemIntestinal MucosaInterleukin 6Autocrine signallingMice KnockoutbiologyInterleukin-6Reverse Transcriptase Polymerase Chain ReactionReceptor Transforming Growth Factor-beta Type IIHistologymedicine.diseaseImmunohistochemistryReceptors Interleukin-6DNA-Binding ProteinsDisease Models AnimalInfectious DiseasesTumor progressionImmunologyColonic NeoplasmsCancer researchbiology.proteinDisease ProgressionTrans-ActivatorsReceptors Transforming Growth Factor betaTransforming growth factorSignal TransductionImmunity
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A key pathogenic role for the STAT1/T-bet signaling pathway in T-cell-mediated liver inflammation.

2003

TH1 cytokines have been suggested to contribute to the pathogenesis of T-cell-mediated liver injury and inflammation. However, the molecular signaling pathways involved in such injury are still poorly understood. In the present study, we investigated the role of the STAT1/T-bet signaling pathway in a murine model of T-cell-mediated liver inflammation induced by the application of concanavalin A (Con A) using newly created STAT1 transgenic mice as well as STAT1- and T-bet-deficient mice. Liver injury induced by Con A was associated with an increase of both pSTAT1 and T-bet levels in the liver. Furthermore, functional studies suggested a pathogenic role for STAT1 in Con A-induced liver injury…

Genetically modified mouseT cellTransgeneT-LymphocytesInflammationMice TransgenicBiologyHepatitisInterferon-gammaMicemedicineConcanavalin AAnimalsInterferon gammaLiver injuryHepatologymedicine.diseasePhosphoproteinsDNA-Binding ProteinsMice Inbred C57BLIRF1medicine.anatomical_structureSTAT1 Transcription FactorLiverImmunologyTrans-ActivatorsSignal transductionmedicine.symptomT-Box Domain Proteinsmedicine.drugInterferon Regulatory Factor-1Signal TransductionTranscription FactorsHepatology (Baltimore, Md.)
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Mutated cylindromatosis gene affects the functional state of dendritic cells

2010

Cylindromatosis gene (CYLD) is a ubiquitously expressed deubiquitinating enzyme, which interacts with members of the NF-κB signaling pathway and attenuates NF-κB and JNK signaling. Here, we report that DC derived from transgenic mice, which solely express a naturally occurring CYLD isoform (CYLD(ex7/8)), display a higher content of nuclear RelB and express elevated levels of NF-κB family members as well as of known NF-κB-target genes comprising costimulatory molecules and pro-inflammatory cytokines, as compared with WT DC. Accordingly, unstimulated CYLD(ex7/8) DC exhibited a significantly higher primary allogenic T-cell stimulatory capacity than WT DC and exerted no tolerogenic activity. Tr…

Genetically modified mouseTransgeneBlotting WesternImmunologyMice TransgenicBiologyDexamethasoneDeubiquitinating enzymeSmall hairpin RNAMiceImmune ToleranceAnimalsImmunology and AllergyGlucocorticoidsMice KnockoutReverse Transcriptase Polymerase Chain ReactionTumor Suppressor ProteinsRELBTranscription Factor RelBNF-kappa BPeripheral toleranceCell DifferentiationDendritic CellsFlow CytometrySpecific Pathogen-Free OrganismsCell biologyIsoenzymesTranscription Factor AP-1MutationKnockout mouseImmunologybiology.proteinRNAFemaleSignal transductionSignal TransductionEuropean Journal of Immunology
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TGFbeta regulates the CD4+CD25+ T-cell pool and the expression of Foxp3 in vivo.

2004

Factors influencing the development of CD4+CD25+ T-cells in vivo are poorly understood. In order to investigate the contribution of TGFbeta1 to the development and function of CD4+CD25+ T-cells, we generated a gain of function mutation resulting in the overexpression of an active form of TGFbeta1 in T-cells under control of the human CD2 promoter. In peripheral lymphoid organs and in the thymus, the frequency of CD4+CD25+ T-cells was increased in transgenic mice. This appeared to be due to an autocrine effect of TGFbeta on T-cells, since concomitant impairment of TGFbeta-signaling in double transgenic mice resulted in a phenotype similar to wild type. In contrast, in single transgenic mice …

Genetically modified mouseTransgeneT cellImmunologyCD2 AntigensMice TransgenicBiologyMiceIn vivoT-Lymphocyte SubsetsTransforming Growth Factor betamedicineImmunology and AllergyAnimalsAutocrine signallingTranscription factorWild typeFOXP3Forkhead Transcription FactorsReceptors Interleukin-2General MedicineMolecular biologyCell biologyInterleukin-10DNA-Binding Proteinsmedicine.anatomical_structureCD4 AntigensInternational immunology
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Association of maternal prenatal smoking GFI1-locus and cardio-metabolic phenotypes in 18,212 adults

2018

Background: DNA methylation at the GFI1-locus has been repeatedly associated with exposure to smoking from the foetal period onwards. We explored whether DNA methylation may be a mechanism that links exposure to maternal prenatal smoking with offspring's adult cardio-metabolic health.Methods: We meta-analysed the association between DNA methylation at GFI1-locus with maternal prenatal smoking, adult own smoking, and cardio-metabolic phenotypes in 22 population-based studies from Europe, Australia, and USA (n= 18,212). DNA methylation at the GFI1-locus was measured in whole-blood. Multivariable regression models were fitted to examine its association with exposure to prenatal and own adult s…

Genetics and Molecular Biology (all)MaleNetherlands Twin Register (NTR)0301 basic medicineResearch paperGFI1 protein humanGFI1-locusraskausResearch & Experimental Medicinecardio-metabolic phenotypesBiochemistryEpigenesis GeneticGLOBAL Meth QTL Consortium0302 clinical medicinePregnancySmoke030212 general & internal medicinematernal prenatal smokingDNA METHYLATIONmedia_commonRISK2. Zero hungereducation.field_of_studySmokingta3142General MedicineMiddle Agedgenetics [Transcription Factors]3. Good healthDNA-Binding ProteinsPhenotypeMedicine Research & ExperimentalCARDIOVASCULAR-DISEASEepigenetiikkaPopulation SurveillancePrenatal Exposure Delayed EffectsDNA methylation/dk/atira/pure/sustainabledevelopmentgoals/good_health_and_well_beingFemaleDisease SusceptibilityBIOS ConsortiumMedical GeneticsLife Sciences & BiomedicineAdultmedicine.medical_specialtyOffspringBirth weightPopulationMothersgenetics [DNA-Binding Proteins]ta3111MethylationGeneral Biochemistry Genetics and Molecular BiologyDIET03 medical and health sciencesMedicine General & InternalSDG 3 - Good Health and Well-beingtupakointiGeneral & Internal MedicineInternal medicine/dk/atira/pure/keywords/cohort_studies/netherlands_twin_register_ntr_medicinemedia_common.cataloged_instanceHumansddc:610adverse effects [Maternal Exposure]EXPOSUREEpigeneticsEuropean unioneducationMedicinsk genetikEPIGENOME-WIDE ASSOCIATIONPregnancyBiochemistry Genetics and Molecular Biology (all)Science & Technologybusiness.industryadverse effects [Smoking]DNA Methylationta3121medicine.diseaseBIRTH-WEIGHT030104 developmental biologyEndocrinologyGenetic Locisydän- ja verisuonitauditCpG IslandsCIGARETTE-SMOKINGCESSATIONEnergy Metabolismmetabolism [Myocardium]businessBody mass indexBiomarkersTranscription FactorsEBioMedicine
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Factors associated with first- versus second-generation long-acting antipsychotics prescribed under ordinary clinical practice in Italy

2018

Background For many years, long-acting intramuscular (LAI) antipsychotics have been prescribed predominantly to chronic and severe patients, as a last resort when other treatments failed. Recently, a broader and earlier use of LAIs, particularly second-generation LAIs, has been emphasized. To date, few studies attempted to frame how this change in prescribing took place in real-world practice. Therefore, this study aimed to describe the clinical features of patients prescribed with LAIs, and to explore possible prescribing differences between first- and second-generations LAIs under ordinary clinical practice in Italy. Methods The STAR Network "Depot" Study is an observational, longitudinal…

Genetics and Molecular Biology (all)MalePediatricsEuropean PeopleBipolar DisorderCross-sectional studyEconomicsEpidemiologymedicine.medical_treatmentassessmentviruseslcsh:MedicineSocial SciencesLongitudinal StudieBiochemistryPrescriptionGeographical locations0302 clinical medicineMathematical and Statistical TechniquesBiochemistry Genetics and Molecular Biology (all); Agricultural and Biological Sciences (all)immune system diseasesEpidemiologyMedicine and Health Scienceslong-acting intramuscular (LAI) antipsychotics; clinical practice; assessment; second-generation antipsychotic (SGA) LAIsAntipsychoticsEthnicitiesLongitudinal Studieslcsh:ScienceMultidisciplinaryvirus diseasesDrugsMiddle Agedclinical practiceItalian PeopleEuropePrescriptionsItalyPhysical SciencesAripiprazoleFemaleBivariate AnalysisStatistics (Mathematics)medicine.drugHumanResearch ArticleAntipsychotic AgentsEmploymentAdultmedicine.medical_specialtyAdolescentResearch and Analysis Methods03 medical and health sciencesMental Health and PsychiatrymedicineHumansPaliperidoneBipolar disorderEuropean UnionStatistical MethodsAntipsychoticCross-Sectional StudiePharmacologyRisperidoneBiochemistry Genetics and Molecular Biology (all)business.industryMood Disorderslcsh:Rmedicine.disease030227 psychiatryAntipsychotic AgentCross-Sectional StudiesAgricultural and Biological Sciences (all)Labor EconomicsMultivariate AnalysisSchizophreniaObservational studylcsh:QPopulation Groupingslong-acting intramuscular (LAI) antipsychoticsPeople and placesbusiness030217 neurology & neurosurgerysecond-generation antipsychotic (SGA) LAIsMathematicsPLoS ONE
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Ascl1 Coordinately Regulates Gene Expression and the Chromatin Landscape during Neurogenesis

2015

Summary The proneural transcription factor Ascl1 coordinates gene expression in both proliferating and differentiating progenitors along the neuronal lineage. Here, we used a cellular model of neurogenesis to investigate how Ascl1 interacts with the chromatin landscape to regulate gene expression when promoting neuronal differentiation. We find that Ascl1 binding occurs mostly at distal enhancers and is associated with activation of gene transcription. Surprisingly, the accessibility of Ascl1 to its binding sites in neural stem/progenitor cells remains largely unchanged throughout their differentiation, as Ascl1 targets regions of both readily accessible and closed chromatin in proliferatin…

Genetics0303 health sciencesNeurogenesisNeurogenesisDNABiologyGeneral Biochemistry Genetics and Molecular BiologyChromatin remodelingArticleCell biologyChromatin03 medical and health sciences0302 clinical medicinelcsh:Biology (General)[SDV.BBM] Life Sciences [q-bio]/Biochemistry Molecular Biology[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyAscl1Scaffold/matrix attachment regionEnhancerlcsh:QH301-705.5Transcription factor030217 neurology & neurosurgeryChIA-PET030304 developmental biologyBivalent chromatin
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