Search results for " Knockout"

showing 10 items of 764 documents

Targeting Homer genes using adeno-associated viral vector: lessons learned from behavioural and neurochemical studies.

2008

Over a decade of in-vitro data support a critical role for members of the Homer family of postsynaptic scaffolding proteins in regulating the functional architecture of glutamate synapses. Earlier studies of Homer knockout mice indicated a necessary role for Homer gene products in normal mesocorticolimbic glutamate transmission and behaviours associated therewith. The advent of adeno-associated viral vectors carrying cDNA for, or short hairpin RNA against, specific Homer isoforms enabled the site-directed targeting of Homers to neurons in the brain. This approach has allowed our groups to address developmental issues associated with conventional knockout mice, to confirm active roles for di…

Scaffold proteinSubstance-Related DisordersTransgeneEmotionsGenetic VectorsGlutamic AcidMice TransgenicBiologySynaptic TransmissionArticleViral vectorAdenoviridaeSmall hairpin RNAMiceNeurochemicalHomer Scaffolding ProteinsAnimalsGeneGenes Immediate-EarlyPharmacologyMice KnockoutBehavior AnimalGlutamate receptorGene Transfer TechniquesBrainPsychiatry and Mental healthAlcoholismKnockout mouseMutagenesis Site-DirectedArousalCarrier ProteinsNeuroscienceBehavioural pharmacology
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Regulation of the p19(Arf)/p53 pathway by histone acetylation underlies neural stem cell behavior in senescence-prone SAMP8 mice.

2015

Brain aging is associated with increased neurodegeneration and reduced neurogenesis. B1/neural stem cells (B1-NSCs) of the mouse subependymal zone (SEZ) support the ongoing production of olfactory bulb interneurons, but their neurogenic potential is progressively reduced as mice age. Although age-related changes in B1-NSCs may result from increased expression of tumor suppressor proteins, accumulation of DNA damage, metabolic alterations, and microenvironmental or systemic changes, the ultimate causes remain unclear. Senescence-accelerated-prone mice (SAMP8) relative to senescence-accelerated-resistant mice (SAMR1) exhibit signs of hastened senescence and can be used as a model for the stud…

SenescenceMaleAgingHistonesMiceNeural Stem CellsNeurospheremedicineSubependymal zoneAnimalsstem cell nicheCyclin-Dependent Kinase Inhibitor p19Mice KnockoutNeuronsbiologyNeurodegenerationNeurogenesishistone acetyltransferasesBrainAcetylationCell BiologyOriginal Articlesmedicine.diseaseGenes p53Neural stem cellChromatinCell biologyadult neurogenesisOxidative StressHistoneImmunologybiology.proteinProtein Processing Post-TranslationalSAMP8 micehistone deacetylasesAging cell
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Host-Nonspecific Iron Acquisition Systems and Virulence in the Zoonotic Serovar of Vibrio vulnificus

2014

ABSTRACT The zoonotic serovar of Vibrio vulnificus (known as biotype 2 serovar E) is the etiological agent of human and fish vibriosis. The aim of the present work was to discover the role of the vulnibactin- and hemin-dependent iron acquisition systems in the pathogenicity of this zoonotic serovar under the hypothesis that both are host-nonspecific virulence factors. To this end, we selected three genes for three outer membrane receptors ( vuuA , a receptor for ferric vulnibactin, and hupA and hutR , two hemin receptors), obtained single and multiple mutants as well as complemented strains, and tested them in a series of in vitro and in vivo assays, using eels and mice as animal models. Th…

SerotypeVirulence FactorsSequence analysisIronImmunologyVirulenceVibrio vulnificusBiologyMicrobiologyMicrobiologyGene Knockout TechniquesMiceVibrio InfectionsAnimalsNatural reservoirOxazolesVibrio vulnificusGeneMice Inbred BALB CVirulenceGenetic Complementation TestMembrane Transport ProteinsBacterial Infectionsbiology.organism_classificationAmidesDisease Models AnimalInfectious DiseasesVibrio InfectionsHeminParasitologyBacterial outer membraneInfection and Immunity
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Tumor protein 53-induced nuclear protein 1 expression is repressed by miR-155, and its restoration inhibits pancreatic tumor development.

2007

Pancreatic cancer is a disease with an extremely poor prognosis. Tumor protein 53-induced nuclear protein 1 ( TP53INP1 ) is a proapoptotic stress-induced p53 target gene. In this article, we show by immunohistochemical analysis that TP53INP1 expression is dramatically reduced in pancreatic ductal adenocarcinoma (PDAC) and this decrease occurs early during pancreatic cancer development. TP53INP1 reexpression in the pancreatic cancer-derived cell line MiaPaCa2 strongly reduced its capacity to form s.c., i.p., and intrapancreatic tumors in nude mice. This anti-tumoral capacity is, at least in part, due to the induction of caspase 3-mediated apoptosis. In addition, TP53INP1 −/− mouse embryonic…

Settore MED/06 - Oncologia MedicaTransplantation HeterologousGene ExpressionMice NudeMicePancreatic tumorPancreatic cancerCell Line TumormicroRNAGene expressionmedicineAnimalsHumansRNA NeoplasmNuclear proteinCaspaseHeat-Shock ProteinsMice KnockoutMultidisciplinarybiologyBase Sequenceapoptosis pancreatic cancer ponasterone A tumor suppressor micro RNANuclear ProteinsBiological Sciencesmedicine.diseaseTransplantationPancreatic NeoplasmsMicroRNAsCell Transformation NeoplasticApoptosisCancer researchbiology.proteinTumor Suppressor Protein p53Carrier ProteinsNeoplasm TransplantationCarcinoma Pancreatic DuctalProceedings of the National Academy of Sciences of the United States of America
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A core cochlear phenotype in USH1 mouse mutants implicates fibrous links of the hair bundle in its cohesion, orientation and differential growth

2008

The planar polarity and staircase-like pattern of the hair bundle are essential to the mechanoelectrical transduction function of inner ear sensory cells. Mutations in genes encoding myosin VIIa, harmonin, cadherin 23,protocadherin 15 or sans cause Usher syndrome type I (USH1, characterized by congenital deafness, vestibular dysfunction and retinitis pigmentosa leading to blindness) in humans and hair bundle disorganization in mice. Whether the USH1 proteins are involved in common hair bundle morphogenetic processes is unknown. Here, we show that mouse models for the five USH1 genetic forms share hair bundle morphological defects. Hair bundle fragmentation and misorientation (25-52° mean ki…

Stereocilia (inner ear)Cadherin Related ProteinsProtocadherinCell Cycle ProteinsNerve Tissue ProteinsMyosinsBiologyMechanotransduction CellularMiceCDH23Pregnancyotorhinolaryngologic diseasesmedicineAnimalsHumansInner earProtein PrecursorsMolecular BiologyActinMice KnockoutCadherinDyneinsAnatomyCadherinsMice Mutant StrainsCochleaCell biologyCytoskeletal ProteinsDisease Models AnimalPhenotypemedicine.anatomical_structureMyosin VIIaMicroscopy Electron ScanningFemalesense organsCarrier ProteinsUsher SyndromesTip linkPCDH15Developmental BiologyDevelopment
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Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
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CB(1) signaling in forebrain and sympathetic neurons is a key determinant of endocannabinoid actions on energy balance

2010

The endocannabinoid system (ECS) plays a critical role in obesity development. The pharmacological blockade of cannabinoid receptor type 1 (CB(1)) has been shown to reduce body weight and to alleviate obesity-related metabolic disorders. An unsolved question is at which anatomical level CB(1) modulates energy balance and the mechanisms involved in its action. Here, we demonstrate that CB(1) receptors expressed in forebrain and sympathetic neurons play a key role in the pathophysiological development of diet-induced obesity. Conditional mutant mice lacking CB(1) expression in neurons known to control energy balance, but not in nonneuronal peripheral organs, displayed a lean phenotype and res…

Sympathetic Nervous SystemPhysiologymedicine.medical_treatmentHUMDISEASEFluorescent Antibody TechniqueBody TemperatureMice0302 clinical medicineReceptor Cannabinoid CB1Cannabinoid receptor type 1ReceptorIn Situ HybridizationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionCB(1)ThermogenesisEndocannabinoid systemOBESITYCB1 knock outlipids (amino acids peptides and proteins)CB(1); CANNABINOID RECEPTOR; OBESITY; ENDOCANNABINOID SYSTEM; METABOLIC DISORDERSSignal Transductionmedicine.medical_specialtyforebrainImmunoblottingCitrate (si)-SynthaseIn situ hybridizationHyperphagiaBiologyDNA MitochondrialModels BiologicalENDOCANNABINOID SYSTEMMOLNEURONO03 medical and health sciencesProsencephalonLipid oxidationInternal medicineMETABOLIC DISORDERSmedicineAnimalsMolecular BiologyCANNABINOID RECEPTOR030304 developmental biologyAnalysis of VarianceX-Ray MicrotomographyCell Biologyendocannabinoidenergy balanceEndocrinologynervous systemsympathetic neuronsForebrainCannabinoidEnergy Metabolismendocannabinoid; forebrain; sympathetic neurons; energy balance; CB1 knock outNeuroscienceThermogenesis030217 neurology & neurosurgery
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Vulnerability of peripheral catecholaminergic neurons to MPTP is not regulated by alpha-synuclein.

2010

Although generally considered a prototypical movement disorder, Parkinson's disease is commonly associated with a broad-spectrum of non-motor symptoms, including autonomic dysfunctions caused by significant alterations in catecholaminergic neurons of the peripheral sympathetic nervous system. Here we present evidence that alpha-synuclein is highly expressed by sympathetic ganglion neurons throughout embryonic and postnatal life and that it is found in tyrosine hydroxylase-positive sympathetic fibers innervating the heart of adult mice. However, mice deficient in alpha-synuclein do not exhibit any apparent alterations in sympathetic development. Sympathetic neurons isolated from mouse embryo…

Sympathetic nervous system1-Methyl-4-phenylpyridiniumα-Synuclein knockoutTyrosine 3-MonooxygenaseNeurotoxinsNeurotrophic factorSubstantia nigraBiologylcsh:RC321-571chemistry.chemical_compoundMiceCatecholaminesSympathetic Fibers PostganglionicParkinsonian DisordersNeurotrophic factorsmedicineNeurotoxinAutonomic gangliaAnimalslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCells CulturedNeuronsGanglia SympatheticCell DeathMPTPSympathetic ganglionMice Mutant Strainsnervous system diseasesMPP+medicine.anatomical_structureNeurologychemistrynervous system1-Methyl-4-phenyl-1236-tetrahydropyridinePeripheral nervous systemSympathetic nervous systemNerve Degenerationalpha-SynucleinCatecholaminergic cell groupsPeripheral nervous systemNeuroscienceNeurobiology of disease
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IL-23 receptor regulates unconventional IL-17-producing T cells that control bacterial infections.

2010

AbstractIL-23 plays an important role in autoimmune tissue inflammation and induces the generation of not fully characterized effector cells that mediate protection against pathogens. In this paper, we established the essential role of IL-23R in the host response against intracellular pathogens. IL-23 was critical for the expansion or maintenance of γδ and double negative (DN) αβ T cells. These cells were rapidly recruited to the site of infection and produced large amounts of IL-17, IFN-γ, and TNF-α. Notably, DN T cells transferred into L. monocytogenes-infected RAG2−/− mice prevented bacterial growth, confirming their protective role against intracellular pathogens. Our results show that …

T cellCD8 AntigensReceptors Antigen T-Cell alpha-betaImmunologyMice NudeMice TransgenicBiologyArticleImmunophenotypingInterferon-gammaMiceImmune systemAntigenCell MovementT-Lymphocyte SubsetsmedicineImmunology and AllergyAnimalsInterferon gammaListeriosisCells CulturedMice KnockoutEffectorTumor Necrosis Factor-alphaIntracellular parasiteInterleukin-17Receptors Antigen T-Cell gamma-deltaReceptors InterleukinCoculture TechniquesCell biologymedicine.anatomical_structureImmunologyCD4 AntigensInterleukin-23 Subunit p19Tumor necrosis factor alphaInterleukin 17Peritoneummedicine.drugJournal of immunology (Baltimore, Md. : 1950)
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Uptake of Leishmania major by dendritic cells is mediated by Fcγ receptors and facilitates acquisition of protective immunity

2006

Uptake of Leishmania major by dendritic cells (DCs) results in activation and interleukin (IL)-12 release. Infected DCs efficiently stimulate CD4- and CD8- T cells and vaccinate against leishmaniasis. In contrast, complement receptor 3-dependent phagocytosis of L. major by macrophages (MPhi) leads exclusively to MHC class II-restricted antigen presentation to primed, but not naive, T cells, and no IL-12 production. Herein, we demonstrate that uptake of L. major by DCs required parasite-reactive immunoglobulin (Ig)G and involved FcgammaRI and FcgammaRIII. In vivo, DC infiltration of L. major-infected skin lesions coincided with the appearance of antibodies in sera. Skin of infected B cell-de…

T cellImmunologyAntigen presentationLeishmaniasis CutaneousMacrophage-1 AntigenPriming (immunology)Complement receptorArticleImmunoglobulin GMicePhagocytosismedicineAnimalsImmunology and AllergyLeishmania majorCells CulturedLeishmania majorMice KnockoutB-LymphocytesMice Inbred BALB CbiologyMacrophagesReceptors IgGArticlesDendritic Cellsbiology.organism_classificationMice Inbred C57BLmedicine.anatomical_structureImmunoglobulin GImmunologybiology.proteinInterleukin 12CD8Journal of Experimental Medicine
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