Search results for " Transgenic"

showing 10 items of 522 documents

n-3 polyunsaturated fatty acids and HER2-positive breast cancer: interest of the fat-1 transgenic mouse model over conventional dietary supplementati…

2013

Overexpression of the tyrosine kinase receptor ErbB2/HER2/Neu, occurs in 25%-30% of invasive breast cancer (BC) with poor patient prognosis. Even if numerous studies have shown prevention of breast cancer by n-3 fatty acid intake, the experimental conditions under which n-3 fatty acids exert their protective effect have been variable from study to study, preventing unifying conclusions. Due to confounding factors, inconsistencies still remain regarding protective effects of n-3 polyunsaturated fatty acids (PUFA) on BC. When animals are fed with dietary supplementation in n-3 fatty acids (the traditional approach to modify tissue content and decrease the n-6/n-3 ratio) complex dietary intera…

Genetically modified mouseFatty Acid Desaturasesmedicine.medical_specialtyReceptor ErbB-2Breast NeoplasmsMice TransgenicBiologyBiochemistryReceptor tyrosine kinaseMiceBreast cancerInternal medicineFatty Acids Omega-3medicineAnimalsAnticarcinogenic AgentsHumansDietary supplementationCaenorhabditis elegans Proteinschemistry.chemical_classificationConfoundingFatty acidGeneral Medicinemedicine.disease3. Good healthDisease Models AnimalEndocrinologychemistryDietary Supplementsbiology.proteinFemaleSignal transductionPolyunsaturated fatty acidBiochimie
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Glycosylation deficiency at either one of the two glycan attachment sites of cellular prion protein preserves susceptibility to bovine spongiform enc…

2004

The conversion into abnormally folded prion protein (PrP) plays a key role in prion diseases. PrP(C) carries two N-linked glycan chains at amino acid residues 180 and 196 (mouse). Previous in vitro data indicated that the conversion process may not require glycosylation of PrP. However, it is conceivable that these glycans function as intermolecular binding sites during the de novo infection of cells on susceptible organisms and/or play a role for the interaction of both PrP isoforms. Such receptor-like properties could contribute to the formation of specific prion strains. However, in earlier studies, mutations at the glycosylation sites of PrP led to intracellular trafficking abnormalitie…

Genetically modified mouseGlycanGlycosylationGlycosylationPrionsanimal diseasesBovine spongiform encephalopathyMutantBlotting WesternScrapieMice TransgenicCHO CellsCell SeparationBiologyBiochemistryCell LinePrion Diseaseschemistry.chemical_compoundMicePolysaccharidesCell Line TumorCricetinaemedicineAnimalsImmunoprecipitationProtein IsoformsBiotinylationDisulfidesTransgenesCloning MolecularMolecular BiologyBinding SitesWild typeBrainCell Biologymedicine.diseaseFlow CytometryVirologyMolecular biologyIn vitronervous system diseasesEncephalopathy Bovine SpongiformMice Inbred C57BLchemistryMutationbiology.proteinCattleScrapieThe Journal of biological chemistry
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Constitutive and inducible expression of CYP enzymes in immortal hepatocytes derived from SV40 transgenic mice

2003

1. The expression of liver-specific transcription factors and cytochrome P450 (CYP) enzymes have been studied in three new hepatocyte-like cell lines derived from SV Delta 202 transgenic mice: AMH-Delta 202 (adult mouse hepatocytes), TAMH-Delta 202 (tumour-derived adult mouse hepatocytes) and NMH-Delta 202 (newborn mouse hepatocytes). 2. mRNA levels of liver-enriched transcription factors such as D-element binding protein (DBP), liver-enriched transcription activating protein (LAP) and the hepatic nuclear factors (HNF) 1, 2 and 3 in all Delta 202 transgenic hepatocyte lines were similar to those in the wild-type liver and in primary mouse hepatocytes. 3. Analysis of basal CYP activities and…

Genetically modified mouseHealth Toxicology and MutagenesisTransgeneGene ExpressionMice TransgenicBiologyHydroxylationToxicologyBiochemistryDexamethasoneCell LineMiceCytochrome P-450 Enzyme SystemGene expressionmedicineAnimalsTestosteroneRNA MessengerTranscription factorPharmacologyEthanolCytochrome P450General MedicineCYP2E1Molecular biologymedicine.anatomical_structureLiverCell cultureEnzyme InductionPhenobarbitalHepatocyteHepatocytesbiology.proteinRifampinMethylcholanthreneTranscription FactorsXenobiotica
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IFN? expression inhibits LHBs storage disease and ground glass hepatocyte appearance, but exacerbates inflammation and apoptosis in HBV surface prote…

2006

BACKGROUND/AIMS Interferon gamma (IFNgamma) controls hepatitis B virus replication. As systemic application may cause severe adverse effects, approaches of liver-directed IFNgamma gene therapy may represent an attractive alternative for treatment of chronic viral hepatitis B and thus needs testing in vivo in suitable animal models. METHODS We therefore crossbred Alb-1HBV transgenic mice overexpressing the large HBV surface protein (LHBs) in their livers and developing LHBs storage disease and ground glass hepatocyte appearance with SAP-IFNgamma transgenic animals previously shown to exhibit constitutive hepatic IFNgamma expression, and analyzed the resulting double-transgenic offspring. RES…

Genetically modified mouseHepatitis B virusHepatitis B Surface AntigensHepatologyGenetic enhancementTransgeneApoptosisMice TransgenicGround glass hepatocyteGenetic TherapyBiologymedicine.disease_causePeripheral blood mononuclear cellMice Inbred C57BLInterferon-gammaMiceHepatitis B ChronicLiverApoptosisImmunologyHepatocytesmedicineAnimalsInterferon gammamedicine.drugLiver International
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Cutting Edge: IL-6–Driven Immune Dysregulation Is Strictly Dependent on IL-6R α-Chain Expression

2020

Abstract IL-6 binds to the IL-6R α-chain (IL-6Rα) and signals via the signal transducer gp130. Recently, IL-6 was found to also bind to the cell surface glycoprotein CD5, which would then engage gp130 in the absence of IL-6Rα. However, the biological relevance of this alternative pathway is under debate. In this study, we developed a mouse model, in which murine IL-6 is overexpressed in a CD11c-Cre–dependent manner. Transgenic mice developed a lethal immune dysregulation syndrome with increased numbers of Ly-6G+ neutrophils and Ly-6Chi monocytes/macrophages. IL-6 overexpression promoted activation of CD4+ T cells while suppressing CD5+ B-1a cell development. However, additional ablation of …

Genetically modified mouseImmunologyInflammationMice Transgenicmedicine.disease_cause03 medical and health sciencesMice0302 clinical medicineRare DiseasesmedicineImmunology and AllergyAnimals2.1 Biological and endogenous factorsInflammatory and Immune SystemReceptorSTAT3biologyCell growthChemistryInterleukin-6Immune dysregulationGlycoprotein 130Receptors Interleukin-6Cell biologybiology.proteinAlternative complement pathwaymedicine.symptom030215 immunologySignal TransductionThe Journal of Immunology
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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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Spontaneous hepatic fibrosis in transgenic mice overexpressing PDGF-A.

2008

Platelet derived growth factor (PDGF) plays a central role in repair mechanisms after acute and chronic tissue damage. To further evaluate the role of PDGF-A in liver fibrogenesis in vivo, we generated transgenic mice with hepatocyte-specific overexpression of PDGF-A using the CRP-gene promoter. Transgenic but not wildtype mice showed expression of PDGF-A mRNA in the liver. Hepatic PDGF-A overexpression was accompanied by a significant increase in hepatic procollagen III mRNA expression as well as TGF-beta1 expression. Liver histology showed increased deposition of extracellular matrix in transgenic but not in wildtype mice. PDGF-A-transgenic mice showed positive sinusoidal staining for alp…

Genetically modified mouseLiver CirrhosisPlatelet-derived growth factorTransgeneGene ExpressionMice TransgenicTransforming Growth Factor beta1chemistry.chemical_compoundMiceFibrosisGeneticsmedicineAnimalsHumansRNA MessengerPlatelet-Derived Growth FactorbiologyGeneral Medicinemedicine.diseaseMolecular biologyRecombinant ProteinsC-Reactive ProteinCollagen Type IIIchemistryLiverHepatic stellate cellbiology.proteinHepatic fibrosisTyrosine kinasePlatelet-derived growth factor receptorSignal TransductionGene
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A Novel 1,4-Dihydropyridine Derivative Improves Spatial Learning and Memory and Modifies Brain Protein Expression in Wild Type and Transgenic APPSweD…

2015

Ca2+ blockers, particularly those capable of crossing the blood-brain barrier (BBB), have been suggested as a possible treatment or disease modifying agents for neurodegenerative disorders, e.g., Alzheimer's disease. The present study investigated the effects of a novel 4-(N-dodecyl) pyridinium group-containing 1,4-dihydropyridine derivative (AP-12) on cognition and synaptic protein expression in the brain. Treatment of AP-12 was investigated in wild type C57BL/6J mice and transgenic Alzheimer's disease model mice (Tg APPSweDI) using behavioral tests and immunohistochemistry, as well as mass spectrometry to assess the blood-brain barrier (BBB) penetration. The data demonstrated the ability …

Genetically modified mouseMalePathologymedicine.medical_specialtyDihydropyridinesTime Factorsmedicine.drug_classTransgeneSpatial Learninglcsh:MedicineMice TransgenicBlood–brain barrierAnxiolyticGyrus CinguliHippocampus03 medical and health sciences0302 clinical medicineHomer Scaffolding ProteinsMemorymedicineAnimalsHumanslcsh:Science030304 developmental biology0303 health sciencesMultidisciplinaryAmyloid beta-PeptidesGlutamate Decarboxylaselcsh:RDihydropyridineWild typeBrainmedicine.disease3. Good healthMice Inbred C57BLmedicine.anatomical_structureAnti-Anxiety AgentsBlood-Brain BarrierSynaptic plasticitylcsh:QAlzheimer's diseaseCarrier ProteinsNeuroscience030217 neurology & neurosurgerymedicine.drugResearch ArticlePloS one
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Aβ and tau toxicities in Alzheimer’s are linked via oxidative stress-induced p38 activation: Protective role of vitamin E

2014

AbstractOxidative stress is a hallmark of Alzheimer’s disease (AD). We propose that rather than causing damage because of the action of free radicals, oxidative stress deranges signaling pathways leading to tau hyperphosphorylation, a hallmark of the disease. Indeed, incubation of neurons in culture with 5 µM beta-amyloid peptide (Aβ) causes an activation of p38 MAPK (p38) that leads to tau hyperphosphorylation. Inhibition of p38 prevents Aβ-induced tau phosphorylation. Aβ-induced effects are prevented when neurons are co-incubated with trolox (the water-soluble analog of vitamin E).We have confirmed these results in vivo, in APP/PS1 double transgenic mice of AD. We have found that APP/PS1 …

Genetically modified mouseMalemedicine.medical_specialtyCell signalingAntioxidantP-p38p38 mitogen-activated protein kinasesmedicine.medical_treatmentClinical BiochemistryMice Transgenictau ProteinsBiologyBeta-amyloidmedicine.disease_causeProtective AgentsBiochemistryHippocampusp38 Mitogen-Activated Protein KinasesArticlechemistry.chemical_compoundMiceAlzheimer DiseaseInternal medicinemental disordersmedicineVitamin EAnimalsPhosphorylationlcsh:QH301-705.5Cells CulturedNeuronslcsh:R5-920Amyloid beta-PeptidesVitamin EOrganic Chemistrymedicine.diseaseRatsDisease Models AnimalOxidative StressEndocrinologylcsh:Biology (General)chemistryTroloxAlzheimer's diseaseAntioxidantlcsh:Medicine (General)Oxidative stressRedox Biology
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