Search results for " Transgenic"

showing 10 items of 522 documents

Influence of ADAM10 on prion protein processing and scrapie infectiosity in vivo.

2009

Abstract Both the cellular prion protein (PrPc) and the amyloid precursor protein (APP) are physiologically subjected to complex proteolytic processing events. While for APP the proteinases involved – alpha-, beta- and gamma-secretase – have been identified in vitro and in vivo, the cleavage of PrPc by now has been linked only to the shedding activity of the metalloproteinase ADAM10 and/or ADAM17 in cell culture. Here we show that neuronal overexpression of the alpha-secretase ADAM10 in mice reduces all PrPc species detected in the brain instead of leading to enhanced amounts of specific cleavage products of PrPc. Additionally, the incubation time of mice after scrapie infection is signific…

Prionsanimal diseasesADAM10Molecular Sequence DataPrion diseaseScrapieMice Transgeniclcsh:RC321-571ADAM10 ProteinMiceIn vivomental disordersNeurotoxicitymedicineAmyloid precursor proteinAnimalsHumansGliosisAmino Acid Sequencealpha-Secretaselcsh:Neurosciences. Biological psychiatry. NeuropsychiatrySheddingMetalloproteinasebiologyChemistryBrainMembrane ProteinsMolecular biologyIn vitronervous system diseasesMice Inbred C57BLADAM ProteinsNeurologyAlpha secretaseGliosisbiology.proteinCattlemedicine.symptomAmyloid Precursor Protein SecretasesProtein Processing Post-TranslationalScrapieNeurobiology of disease
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Acute organ failure following the loss of anti-apoptotic cellular FLICE-inhibitory protein involves activation of innate immune receptors

2014

Apoptosis signaling is involved in both physiological tissue homeostasis and acute and chronic diseases. The role of regulatory apoptosis signaling molecules and their organ-specific functions are less defined. Therefore, we investigated the loss of the anti-apoptotic cellular FLICE-inhibitory protein (cFLIP) and the mechanisms of the resulting lethal organ failure in vivo using inducible knockout mice. These were generated by crossing floxed cFLIP mice to a tamoxifen inducible Rosa26-creERT2 mouse strain. Death following global loss of cFLIP resulted from liver failure, accumulation of M1-polarized macrophages and accompanying hepatic cell death and inflammation. Apoptosis was also promine…

Programmed cell deathCASP8 and FADD-Like Apoptosis Regulating ProteinMice TransgenicInflammationBiologyMiceImmune systemmedicineAnimalsMolecular BiologyTissue homeostasisOriginal PaperInnate immune systemMacrophagesMembrane ProteinsCell BiologyLiver Failure AcuteImmunity InnateCell biologyToll-Like Receptor 4TransplantationApoptosisToll-Like Receptor 9Stimulator of interferon genesHepatocytesmedicine.symptomCell Death & Differentiation
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Polyglutamine toxicity induces rod photoreceptor division, morphological transformation or death in Spinocerebellar ataxia 7 mouse retina

2010

In neurodegenerative disorders caused by polyglutamine (polyQ) expansion, polyQ toxicity is thought to trigger a linear cascade of successive degenerative events leading to neuronal death. To understand how neurons cope with polyQ toxicity, we studied a Spinocerebellar ataxia 7 (SCA7) mouse which expresses polyQ-expanded ATXN7 only in rod photoreceptors. We show that in response to polyQ toxicity, SCA7 rods go through a range of radically different cell fates, including apoptotic and non-apoptotic cell death, cell migration, morphological transformation into a round cell or, most remarkably, cell division. The temporal profile of retinal remodeling indicates that some degenerative pathways …

Programmed cell deathCell divisionProliferationPopulationMice TransgenicNerve Tissue ProteinsBiologylcsh:RC321-571Mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineCell MovementRetinal Rod Photoreceptor CellsmedicineAnimalsSpinocerebellar AtaxiasNeurodegenerationeducationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCell ShapeComputingMilieux_MISCELLANEOUSSpinocerebellar ataxia 7030304 developmental biologyAtaxin-7Mice Knockout0303 health sciencesRetinaeducation.field_of_studyPhotoreceptorCell DeathRetinal DegenerationNeurodegenerationRetinalmedicine.diseaseRemodelingMice Inbred C57BLmedicine.anatomical_structureNeurologyProteotoxicitychemistryNerve DegenerationSpinocerebellar ataxia[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]Apoptosis Regulatory ProteinsPeptidesPolyglutamineNeuroscience030217 neurology & neurosurgery
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Pro-inflammatory T helper 17 directly harms oligodendrocytes in neuroinflammation.

2021

Significance Multiple sclerosis (MS) is a neuroinflammatory, demyelinating disease that represents one of the most frequent causes of irreversible disability in young adults. Treatment options to halt disability are limited. We discovered that T helper (Th)17 cells in contact with oligodendrocytes produce higher levels of glutamate and induce significantly greater oligodendrocyte damage than their Th2 counterpart. Blockade of CD29, which is linked to glutamate release pathways and expressed in high levels on Th17 cells, preserved human oligodendrocyte processes from Th17-mediated injury. Our data thus provide evidence for the direct and deleterious attack of Th17 cells on the myelin compart…

Programmed cell deathEncephalomyelitis Autoimmune ExperimentalCentral nervous systemFreund's AdjuvantoligodendrocytesMice Transgenicglutamate03 medical and health sciencesMyelinMice0302 clinical medicineImmunology and Inflammationintravital microscopymedicineAnimalsNeuroinflammation030304 developmental biologyInflammationMice Knockout0303 health sciencesMultidisciplinaryChemistryMultiple sclerosisGlutamate receptorMembrane ProteinsCD29Biological SciencesCD29 blockademedicine.disease420Oligodendrocyte3. Good healthCell biologyDNA-Binding ProteinsMice Inbred C57BLOligodendrogliamedicine.anatomical_structurePertussis ToxinTh17 CellsMyelin-Oligodendrocyte Glycoprotein030217 neurology & neurosurgeryProceedings of the National Academy of Sciences of the United States of America
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BAG3 mediates chaperone-based aggresome-targeting and selective autophagy of misfolded proteins.

2010

Increasing evidence indicates the existence of selective autophagy pathways, but the manner in which substrates are recognized and targeted to the autophagy system is poorly understood. One strategy is transport of a particular substrate to the aggresome, a perinuclear compartment with high autophagic activity. In this paper, we identify a new cellular pathway that uses the specificity of heat-shock protein 70 (Hsp70) to misfolded proteins as the basis for aggresome-targeting and autophagic degradation. This pathway is regulated by the stress-induced co-chaperone Bcl-2-associated athanogene 3 (BAG3), which interacts with the microtubule-motor dynein and selectively directs Hsp70 substrates …

Protein FoldingRecombinant Fusion ProteinsDyneinGreen Fluorescent ProteinsAggrephagyMice TransgenicBAG3BiochemistryMiceJUNQ and IPODChlorocebus aethiopsGeneticsAutophagyAnimalsHumansPoint MutationHSP70 Heat-Shock ProteinsMolecular BiologyAdaptor Proteins Signal TransducingSequence DeletionInclusion BodiesMotor NeuronsbiologySuperoxide DismutaseAutophagyScientific ReportsDyneinsTransport proteinCell biologyProtein TransportAggresomeHEK293 CellsSpinal CordChaperone (protein)COS Cellsbiology.proteinApoptosis Regulatory ProteinsProteasome InhibitorsEMBO reports
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Wild-type Cu/Zn superoxide dismutase (SOD1) does not facilitate, but impedes the formation of protein aggregates of amyotrophic lateral sclerosis cau…

2009

Aggregation of Cu/Zn superoxide dismutase (SOD1) is a hallmark of a subset of familial amyotrophic lateral sclerosis (ALS) cases. The expression of wild-type SOD1 [SOD(hWT)] surprisingly exacerbates the phenotype of mutant SOD1 in vivo. Here we studied whether SOD1(hWT) may affect mutant SOD1 aggregation by employing fluorescence microscopy techniques combined with lifetime-based Förster resonance energy transfer (FRET). Only a very minor fraction of SOD1(hWT) was observed in aggregates induced by mutant SOD1(G37R), SOD1(G85R) or SOD1(G93C). Quite in contrast, co-expression of SOD(hWT) reduced the amount of mutant SOD1 in the aggregate fraction. Furthermore, we did not detect endogenous mou…

Protein Foldinganimal diseasesSOD1HeterodimerizationMice TransgenicEndogenyProtein aggregationCell Linelcsh:RC321-571MiceSuperoxide Dismutase-1In vivoFluorescence microscopeAnimalsHumanslcsh:Neurosciences. Biological psychiatry. NeuropsychiatrySuperoxide DismutaseChemistryWild typenutritional and metabolic diseasesAmyotrophic lateral sclerosisPhenotypeMolecular biologynervous system diseasesFörster resonance energy transferSolubilitynervous systemNeurologyFLIM-based FRETMutationProtein MultimerizationProtein aggregationNeurobiology of Disease
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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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CD34+ progenitor to endothelial cell transition in post-pneumonectomy angiogenesis.

2012

In many species, pneumonectomy triggers compensatory lung growth that results in an increase not only in lung volume, but also in alveolar number. Whether the associated alveolar angiogenesis involves the contribution of blood-borne progenitor cells is unknown. To identify and characterize blood-borne progenitor cells contributing to lung growth after pneumonectomy in mice, we studied wild-type and wild-type/green fluorescence protein (GFP) parabiotic mice after left pneumonectomy. Within 21 days of pneumonectomy, a 3.2-fold increase occurred in the number of lung endothelial cells. This increase in total endothelial cells was temporally associated with a 7.3-fold increase in the number of …

Pulmonary and Respiratory MedicineTranscriptional ActivationPathologymedicine.medical_specialtyTime FactorsAngiogenesisCellular differentiationClinical BiochemistryGreen Fluorescent ProteinsCD34Neovascularization PhysiologicAntigens CD34Mice TransgenicBiologyMiceVasculogenesisCell MovementmedicineAnimalsRegenerationProgenitor cellPneumonectomyMolecular BiologyLungCell ProliferationStem CellsEndothelial CellsCell DifferentiationCell BiologyArticlesEndothelial stem cellVascular endothelial growth factor BMice Inbred C57BLGene Expression RegulationCancer researchStem cellAmerican journal of respiratory cell and molecular biology
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Amyloid Beta-Mediated Changes in Synaptic Function and Spine Number of Neocortical Neurons Depend on NMDA Receptors

2021

Onset and progression of Alzheimer’s disease (AD) pathophysiology differs between brain regions. The neocortex, for example, is a brain region that is affected very early during AD. NMDA receptors (NMDARs) are involved in mediating amyloid beta (Aβ) toxicity. NMDAR expression, on the other hand, can be affected by Aβ. We tested whether the high vulnerability of neocortical neurons for Aβ-toxicity may result from specific NMDAR expression profiles or from a particular regulation of NMDAR expression by Aβ. Electrophysiological analyses suggested that pyramidal cells of 6-months-old wildtype mice express mostly GluN1/GluN2A NMDARs. While synaptic NMDAR-mediated currents are unaltered in 5xFAD …

QH301-705.5Amyloid betasomatosensory cortexDendritic SpinesMice TransgenicNeocortexSomatosensory systemReceptors N-Methyl-D-AspartateCatalysisArticleInorganic ChemistryAlzheimer Diseasemental disordersmedicineAnimalsBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyNeuronsNeocortexAmyloid beta-PeptidesbiologyPyramidal Cellsmusculoskeletal neural and ocular physiologyOrganic ChemistryWild typeAmyloid betaExcitatory Postsynaptic PotentialsGeneral Medicine5xFADPathophysiologyComputer Science ApplicationsNMDARChemistryElectrophysiologyProtein Subunitsmedicine.anatomical_structurenervous systemKnockout mouseSynapsesbiology.proteinNMDA receptorbiological phenomena cell phenomena and immunityNeuroscienceAlzheimer’s diseasepsychological phenomena and processesInternational Journal of Molecular Sciences
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Inducible and reversible inhibition of mirna-mediated gene repression in vivo

2021

Although virtually all gene networks are predicted to be controlled by miRNAs, the contribution of this important layer of gene regulation to tissue homeostasis in adult animals remains unclear. Gain and loss-of-function experiments have provided key insights into the specific function of individual miRNAs, but effective genetic tools to study the functional consequences of global inhibition of miRNA activity in vivo are lacking. Here we report the generation and characterization of a genetically engineered mouse strain in which miRNA-mediated gene repression can be reversibly inhibited without affecting miRNA biogenesis or abundance. We demonstrate the usefulness of this strategy by invest…

QH301-705.5ScienceGene regulatory networkregenerative medicineMice TransgenicBiologyGeneral Biochemistry Genetics and Molecular BiologyMiceT6BPregnancystem cellsmicroRNAAnimalsHomeostasisRNA-Induced Silencing ComplexRegenerationmolecular biologyGene Regulatory NetworksTransgenesBiology (General)Tissue homeostasisargonautemousemiRNARegulation of gene expressionGeneral Immunology and MicrobiologymicroRNAGeneral NeuroscienceRegeneration (biology)QRRISCmiRISCGeneral MedicineCell BiologyArgonauteStem Cells and Regenerative MedicineCell biologyTNRC6MicroRNAsMedicineFemaleStem cellPeptidesFunction (biology)Research Article
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