Search results for "Knockout mouse"

showing 10 items of 81 documents

Altered morphological and electrophysiological properties of Cajal-Retzius cells in cerebral cortex of embryonic Presenilin-1 knockout mice

2004

Mutations of Presenilin-1 are the major cause of familial Alzheimer's disease. Presenilin-1 knockout (PS1-/-) mice develop severe cortical dysplasia related to human type 2 lissencephaly. This overmigration syndrome has been attributed to the premature loss of Cajal-Retzius cells (CRcs), pioneer neurons required for the termination of radial neuronal migration. To elucidate the potential cellular mechanisms responsible for this premature neuronal loss, we investigated the morphological and electrophysiological properties of visually identified CRcs of wild-type (WT) and PS1-/- mouse brains at embryonic day 16.5. The density of CRcs was substantially reduced in the cerebral cortex of PS1-/-.…

Cell Adhesion Molecules NeuronalNerve Tissue ProteinsBiologyBicucullineMembrane PotentialsGABA AntagonistsMicemental disordersExcitatory Amino Acid AgonistsPresenilin-1medicineAnimalsneoplasms6-Cyano-7-nitroquinoxaline-23-dioneCerebral CortexMice KnockoutNeuronsMembrane potentialExtracellular Matrix ProteinsGABAA receptorStem CellsGeneral NeuroscienceSerine EndopeptidasesExcitatory Postsynaptic PotentialsMembrane ProteinsCortical dysplasiaBicucullineEmbryo Mammalianmedicine.diseaseImmunohistochemistryElectric Stimulationdigestive system diseasesnervous system diseasesCell biologyReelin ProteinElectrophysiologymedicine.anatomical_structure2-Amino-5-phosphonovaleratenervous systemCerebral cortexKnockout mouseExcitatory postsynaptic potentialExcitatory Amino Acid AntagonistsNeurosciencemedicine.drugEuropean Journal of Neuroscience
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Role of the cellular prion protein in oligodendrocyte precursor cell proliferation and differentiation in the developing and adult mouse CNS

2012

There are numerous studies describing the signaling mechanisms that mediate oligodendrocyte precursor cell (OPC) proliferation and differentiation, although the contribution of the cellular prion protein (PrP c) to this process remains unclear. PrP c is a glycosyl-phosphatidylinositol (GPI)-anchored glycoprotein involved in diverse cellular processes during the development and maturation of the mammalian central nervous system (CNS). Here we describe how PrP c influences oligodendrocyte proliferation in the developing and adult CNS. OPCs that lack PrP c proliferate more vigorously at the expense of a delay in differentiation, which correlates with changes in the expression of oligodendrocyt…

Central Nervous SystemTelencephalonMouseCellular differentiationanimal diseasesGene ExpressionHippocampusMice0302 clinical medicineNeural Stem CellsGene expressionMolecular Cell BiologyNeurobiology of Disease and RegenerationCell proliferationNeuronsCerebral CortexMice Knockout0303 health sciencesProliferació cel·lularMultidisciplinaryNeurogenesisQRCell DifferentiationAnimal ModelsNeural stem cell3. Good healthCell biologyOligodendrogliamedicine.anatomical_structureKnockout mouseMedicineFemaleBiologia del desenvolupamentCellular TypesCell DivisionResearch ArticlePrionsNeurogenesisScienceBiologyModels BiologicalCell Growth03 medical and health sciencesModel OrganismsDevelopmental NeuroscienceNeuroglial Developmentmental disordersDevelopmental biologymedicineAnimalsPrPC ProteinsBiology030304 developmental biologyCell ProliferationCell growthLineage markersMolecular DevelopmentOligodendrocytenervous system diseasesMice Inbred C57BLImmunologyOrganism Development030217 neurology & neurosurgeryDevelopmental BiologyNeuroscience
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Analysis of Lipid Experiments (ALEX): A Software Framework for Analysis of High-Resolution Shotgun Lipidomics Data

2013

Global lipidomics analysis across large sample sizes produces high-content datasets that require dedicated software tools supporting lipid identification and quantification, efficient data management and lipidome visualization. Here we present a novel software-based platform for streamlined data processing, management and visualization of shotgun lipidomics data acquired using high-resolution Orbitrap mass spectrometry. The platform features the ALEX framework designed for automated identification and export of lipid species intensity directly from proprietary mass spectral data files, and an auxiliary workflow using database exploration tools for integration of sample information, computat…

Databases FactualComputer scienceData managementlcsh:MedicineBioinformaticscomputer.software_genreMass spectrometryMiceUser-Computer InterfaceData visualizationLipidomicsAnimalslcsh:ScienceInternetMultidisciplinarybusiness.industrylcsh:RBrainLipid-phosphate phosphataseShotgun lipidomicsLipidomeLipidsVisualizationSoftware frameworkKnockout mouselcsh:QData miningbusinesscomputerSoftwareResearch ArticlePLoS ONE
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No effect of C-reactive protein on early atherosclerosis in LDLR-/- / human C-reactive protein transgenic mice

2008

summaryThe association between increased concentrations of C-reactive protein (CRP) and future cardiovascular events is well established. However, it is currently unclear whether this clinical observation represents an epiphenomenon or whether the pentraxin may actively promote the development of atherosclerosis. Experimental studies with knockout mice with a defect in apolipoprotein E (ApoE-/-) have been used to investigate the role of CRP in atherogenesis, but the results obtained have been contradictory so far. Since knockout mice with a defect in low density lipoprotein receptor (LDLR-/-) may represent a better model of atherogenesis compared to ApoE-/- animals, we undertook experiments…

Genetically modified mouseApolipoprotein ETime FactorsGenotypeLipoproteinsTransgeneMice TransgenicBiologyLesionMicemedicineAnimalsHumansComplement ActivationAortaCrosses GeneticMice KnockoutC-reactive proteinAcute-phase proteinHematologyAtherosclerosisDietary FatsLipidsDisease Models AnimalC-Reactive ProteinPhenotypeReceptors LDLImmunologyLDL receptorKnockout mousebiology.proteinlipids (amino acids peptides and proteins)medicine.symptomThrombosis and Haemostasis
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Improved models for animal research

2008

Experimental animal models are critical to understand gene function and human disease. Many rodent models are presently available providing avenues to elucidate gene function and/or to recapitulate specific pathological conditions. To a large extent, successful translation of clinical evidence or analytical data into appropriate mouse models is possible through progress in transgenic or gene deletion technology. Despite these significant improvements, major limitations still exist in manipulating the mouse genome. For this reason and to maximize success, the design and planning of mouse models need good knowledge concerning the requirements and limitations of commonly used strategies and em…

Genetically modified mouseHuman diseaseEmerging technologiesComputer sciencemedia_common.quotation_subjectKnockout mouseExperimental Animal ModelsComputational biologyFunction (engineering)GenomeFunctional genomicsmedia_common
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Chronic inflammatory cardiomyopathy of interferon γ-overexpressing transgenic mice is mediated by tumor necrosis factor-α.

2011

We recently described a model of inflammatory cardiomyopathy in interferon (IFN)-γ overexpressing transgenic mice stably circulating IFN-γ in the serum referred to as SAP–-IFN-γ mice. SAP–IFN-γ transgenic mice show cardiac infiltration by mononuclear leukocytes, culminating in dilated cardiomyopathy characterized by an increase of left ventricular end diastolic diameter and reduction of fractional shortening. We hypothesized that the pathological mechanism underlying SAP–IFN-γ cardiomyopathy might be mediated by (auto)immune processes or tumor necrosis factor (TNF)-α synthesis from IFN-γ–activated macrophages. To verify these hypotheses, we crossed SAP–IFN-γ transgenic mice with immunodefic…

Genetically modified mouseMalemedicine.medical_specialtyMyocarditisTransgeneCardiomyopathyApoptosisAutoimmunityMice TransgenicKaplan-Meier EstimateBiologyAdaptive ImmunityPathology and Forensic MedicineHepatitisInterferon-gammaMiceImmune systemInterferonInternal medicinemedicineAnimalsGene SilencingTumor Necrosis Factor-alphaMacrophagesAlanine Transaminasemedicine.diseaseMyocarditisEndocrinologyPhenotypeEchocardiographyKnockout mouseChronic DiseaseCytokinesTumor necrosis factor alphaFemalemedicine.drugThe American journal of pathology
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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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DNA Repair and Damage Response Following Exposure of Cells to Alkylating Carcinogens

2012

Abstract Alkylating carcinogens are widely distributed in the environment and are present in food, beverages and tobacco. They are also endogenously formed in stomach and gut. These agents induce a dozen different DNA lesions, and some of them have been identified to be carcinogenic, clastogenic, recombinogenic and cytotoxic. A critical DNA adduct is O6-methylguanine (O6MeG). This damage causes mutations and is responsible for most of the carcinogenic effects of simple alkylating agents. At the same time, O6MeG is a highly powerful cytotoxic lesion, giving rise to the induction of apoptosis, necrosis and autophagy. The damage is repaired by the suicide enzyme alkyltransferase (MGMT), which …

GeneticsBiomarkerchemistry.chemical_compoundchemistryDNA repairApoptosisKnockout mouseDNA adductCancer researchBiologyDNACarcinogenAlkyltransferaseSixth International Conference on Environmental Mutagens in Human Populations
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Conditional transgenic mouse models: from the basics to genome-wide sets of knockouts and current studies of tissue regeneration

2008

Many mouse models are currently available, providing avenues to elucidate gene function and to recapitulate specific pathological conditions. To a large extent, successful translation of clinical evidence or analytical data into appropriate mouse models is possible through progress in transgenic or gene-targeting technology. Beginning with a review of standard mouse transgenics and conventional gene targeting, this article will move on to discussing the basics of conditional gene expression: the tetracycline (tet)-off and tet-on systems based on the transactivators tet-controlled transactivator (Tta) and reverse tet-on transactivator (rtTA) that allow downregulation or induction of gene exp…

GeneticsEmbryologyReporter geneGenomeTransgeneBiomedical EngineeringGene targetingCre recombinaseMice TransgenicComputational biologyBiologyMiceGene trappingConditional gene knockoutKnockout mouseAnimalsRegenerationGene knockout
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Increased susceptibility of complement factor B/C2 double knockout mice and mannan-binding lectin knockout mice to systemic infection with Candida al…

2008

Candida albicans is the major cause of systemic fungal infections in immunocompromised patients. We investigated the susceptibility of mice deficient in complement factor B and C2 (Bf/C2-/-), C1q (C1qa-/-), and mannan-binding lectin (MBL)-A (MBL-A) and MBL-C (MBL-A/C-/-) to systemic infection with C. albicans. Animals were infected i.p. with 10(8)C. albicans blastoconidia and monitored for mortality. Bf/C2-/- mice showed high mortality (over 90%) within the study period of 3 weeks. In contrast, mortality in C1qa-/- mice was below 15% whereas that of MBL-A/C-/- mice was 40% (P0.001). Intravenous infection of mice with 8x10(5) blastoconidia resulted in the same trend with Bf/C2-/- mice being …

Immunologychemical and pharmacologic phenomenaOpportunistic InfectionsMannose-Binding LectinBlastoconidiumComplement factor BMicrobiologyMicePhagocytosisSpecies SpecificityCandida albicansAnimalsGenetic Predisposition to DiseaseCandida albicansDouble knockoutComplement ActivationMolecular BiologyMannan-binding lectinMice KnockoutbiologyCandidiasisLectinComplement Pathway Mannose-Binding LectinComplement C2bacterial infections and mycosesbiology.organism_classificationCorpus albicansKnockout mousebiology.proteinComplement Factor BMolecular Immunology
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