Search results for "Genetically modified mouse"

showing 6 items of 106 documents

Extensive characterization of the human DDAH1 transgenic mice

2009

Abstract Purpose of the research Overexpression of the human dimethylarginine dimethylaminohydrolase type 1 (hDDAH1) gene was reported to have beneficial cardiovascular effects in mice. To date, it is unclear whether these effects are related to enhanced metabolic clearance of asymmetric dimethylarginine (ADMA) and l - N G -mono-methyl- l -arginine ( l -NMMA) or increased DDAH1 expression and activity in cardiovascular tissues of hDDAH1 transgenic mice. Principal results DDAH activity (DDAH1 + DDAH2) was found to be markedly increased in aortic and heart tissues but unaltered in liver and kidney tissues of hDDAH1 transgenic as compared to wild-type (WT) mice. In WT mice, DDAH activity was m…

MaleGenetically modified mousemedicine.medical_specialtyEndotheliumArginineTransgeneMice TransgenicArginineNitric OxideGene Expression Regulation EnzymologicAmidohydrolasesMicechemistry.chemical_compoundEnosInternal medicinemedicineAnimalsHumansTissue DistributionRNA MessengerPharmacologyKidneybiologyChemistryArteriosclerosismedicine.diseasebiology.organism_classificationIsoenzymesMice Inbred C57BLmedicine.anatomical_structureEndocrinologyOrgan SpecificityFemaleAsymmetric dimethylarginineSignal TransductionPharmacological Research
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Sensing life: regulation of sensory neuron survival by neurotrophins

2002

Neurotrophins are a family of structurally and functionally related neurotrophic factors which, in mammals, include: nerve growth factor, brain-derived neurotrophic factor, neurotrophin-3 (NT-3), and NT-4/5. In addition to their canonical role in promoting neuronal survival, these molecules appear to regulate multiple aspects of the development of the nervous system in vertebrates, including neuronal differentiation, axon elongation and target innervation, among others. Actions of neurotrophins and of their receptors in vivo are being analyzed by loss-of-function or gain-of-function experiments in mice. Here, we review the phenotypes of the primary sensory system in these mutant mouse strai…

Nervous systemGenetically modified mouseCell SurvivalMice TransgenicSensory systemReceptors Nerve Growth FactorMiceCellular and Molecular NeuroscienceNeurotrophic factorsmedicineAnimalsReceptor trkCNerve Growth FactorsNeurons AfferentAxonMolecular BiologyMice KnockoutPharmacologyMembrane GlycoproteinsbiologyBrain-Derived Neurotrophic FactorCell BiologyAnatomyProtein-Tyrosine KinasesSensory neuronmedicine.anatomical_structureNerve growth factornervous systembiology.proteinMolecular MedicineNeuroscienceSignal TransductionNeurotrophinCellular and Molecular Life Sciences
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Compromised central tolerance of ICA69 induces multiple organ autoimmunity

2014

For reasons not fully understood, patients with an organ-specific autoimmune disease have increased risks of developing autoimmune responses against other organs/tissues. We identified ICA69, a known β-cell autoantigen in Type 1 diabetes, as a potential common target in multi-organ autoimmunity. NOD mice immunized with ICA69 polypeptides exhibited exacerbated inflammation not only in the islets, but also in the salivary glands. To further investigate ICA69 autoimmunity, two genetically modified mouse lines were generated to modulate thymic ICA69 expression: the heterozygous ICA69(del/wt) line and the thymic medullary epithelial cell-specific deletion Aire-ΔICA69 line. Suboptimal central neg…

Primary Sjogren's syndromeGenetically modified mouseImmunologyThyroid GlandAutoimmune diabeteMice TransgenicThymus GlandBiologymedicine.disease_causeAutoantigensArticleSalivary GlandsSettore MED/13 - EndocrinologiaAutoimmune DiseasesAutoimmunityImmune toleranceAutoimmune thyroiditisIslets of LangerhansMiceICA69Mice Inbred NODImmune TolerancemedicineAnimalsImmunology and AllergyThymuAutoimmune thyroiditiNOD miceInflammationAutoimmune diseaseStomachmedicine.diseaseGene Expression RegulationAutoimmune polyendocrine syndromeImmunologyAutoimmune polyendocrine syndromeCentral toleranceJournal of Autoimmunity
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Increased oxidative stress and impaired antioxidant response in Lafora disease.

2014

15 páginas, 10 figuras

ProteomicsGenetically modified mouseAntioxidantmedicine.medical_treatmentNeuroscience (miscellaneous)Proteomic analysisMice TransgenicBiologymedicine.disease_causeBiochemistryAntioxidantsLafora diseaseMiceCellular and Molecular NeuroscienceLaforinPhysiology (medical)AutophagymedicineAnimalsHumansLafora diseaseMice Knockoutchemistry.chemical_classificationReactive oxygen speciesAutophagymedicine.diseaseMalinCell biologyNeurologychemistryBiochemistryOxidative stressMutationAntioxidant enzymesReactive Oxygen SpeciesLaforinOxidative stressIntracellularFree radical biologymedicine
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A novel homologous model for noninvasive monitoring of endometriosis progression.

2017

To date, several groups have generated homologous models of endometriosis through the implantation of endometrial tissue fluorescently labeled by green fluorescent protein (GFP) or tissue from luciferase-expressing transgenic mice into recipient animals, enabling noninvasive monitoring of lesion signal. These models present an advantage over endpoint models, but some limitations persist; use of transgenic mice is laborious and expensive, and GFP presents poor tissue penetration due to the relatively short emission wavelength. For this reason, a homologous mouse model of endometriosis that allows in vivo monitoring of generated lesions over time and mimics human lesions in recipient mice wou…

adenoviral labeling0301 basic medicineGenetically modified mousein vivo monitoringPathologymedicine.medical_specialtynoninvasive modelEndometriosisEndometriosisMice Transgenichomologous mouse modelBiologyEndometriumGreen fluorescent proteinLesion03 medical and health sciencesEndometriumMiceendometriotic lesionsIn vivomedicineAnimalsHumansNeovascularization PathologicDecidualizationCell BiologyGeneral Medicinemedicine.diseaseMice Inbred C57BLDisease Models AnimalLuminescent Proteins030104 developmental biologymedicine.anatomical_structureReproductive MedicineMicroscopy FluorescenceDisease ProgressionFemalemedicine.symptommCherryBiology of reproduction
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Deficiency of Nrf2 accelerates the effector phase of arthritis and aggravates joint disease

2011

14 páginas, 8 figuras, 1 tabla.-- et al.

musculoskeletal diseasesGenetically modified mouseMedicinaNF-E2-Related Factor 2PhysiologyChemokine CXCL1Clinical BiochemistryNitric Oxide Synthase Type IIArthritisMice Transgenicmedicine.disease_causeenvironment and public healthBiochemistryNrf2MicemedicineAnimalsMolecular BiologyGeneral Environmental SciencebiologyInterleukin-6Effectorbusiness.industryArthritisInflammation and degenerationCell Biologyrespiratory systemmedicine.diseaseArthritis ExperimentalInfection and autoimmunity Auto-immunity transplantation and immunotherapy [NCMLS 1]Disease Models AnimalOxidative StressEicosanoidCyclooxygenase 2Rheumatoid arthritisTumor Necrosis FactorsImmunologyOsteocalcinbiology.proteinGeneral Earth and Planetary SciencesJointsTumor necrosis factor alphaImmune Regulation Auto-immunity transplantation and immunotherapy [NCMLS 2]businessOxidation-ReductionHeme Oxygenase-1Oxidative stress
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