Search results for "Knockout"

showing 10 items of 806 documents

A restricted population of CB1 cannabinoid receptors with neuroprotective activity.

2014

The CB1 cannabinoid receptor, the main molecular target of endocannabinoids and cannabis active components, is the most abundant G protein-coupled receptor in the mammalian brain. Of note, CB1 receptors are expressed at the synapses of two opposing (i.e., GABAergic/inhibitory and glutamatergic/excitatory) neuronal populations, so the activation of one and/or another receptor population may conceivably evoke different effects. Despite the widely reported neuroprotective activity of the CB1 receptor in animal models, the precise pathophysiological relevance of those two CB1 receptor pools in neurodegenerative processes is unknown. Here, we first induced excitotoxic damage in the mouse brain b…

MaleCannabinoid receptorPopulationNeurotoxinsExcitotoxicityGlutamic AcidBiologymedicine.disease_causeNeuroprotectionGlutamatergicMiceOrgan Culture TechniquesReceptor Cannabinoid CB1medicineAnimalsHumansGABAergic NeuronsReceptoreducationCaenorhabditis elegans ProteinsAgedCerebral CortexMice KnockoutNeuronseducation.field_of_studyMultidisciplinaryIntegrasesmusculoskeletal neural and ocular physiologyNeurodegenerative DiseasesBiological SciencesMiddle AgedReceptors GABA-AEndocannabinoid systemCorpus Striatumnervous systemGABAergiclipids (amino acids peptides and proteins)FemaleNeurosciencepsychological phenomena and processesEndocannabinoidsSynaptosomesProceedings of the National Academy of Sciences of the United States of America
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CB1 Cannabinoid Receptors and On-Demand Defense Against Excitotoxicity

2003

Abnormally high spiking activity can damage neurons. Signaling systems to protect neurons from the consequences of abnormal discharge activity have been postulated. We generated conditional mutant mice that lack expression of the cannabinoid receptor type 1 in principal forebrain neurons but not in adjacent inhibitory interneurons. In mutant mice,the excitotoxin kainic acid (KA) induced excessive seizures in vivo. The threshold to KA-induced neuronal excitation in vitro was severely reduced in hippocampal pyramidal neurons of mutants. KA administration rapidly raised hippocampal levels of anandamide and induced protective mechanisms in wild-type principal hippocampal neurons. These protecti…

MaleCannabinoid receptorReceptors Drugmedicine.medical_treatment2-ArachidonoylglycerolExcitotoxicityHippocampal formationmedicine.disease_causeHippocampusMicechemistry.chemical_compoundPiperidinesCannabinoid receptor type 1Excitatory Amino Acid AgonistsReceptors Cannabinoidgamma-Aminobutyric AcidMice KnockoutNeuronsKainic AcidMultidisciplinaryBrainEndocannabinoid systemNeuroprotective AgentsMitogen-Activated Protein KinasesRimonabantSignal Transductionmedicine.medical_specialtyKainic acidPolyunsaturated AlkamidesGlutamic AcidMice TransgenicArachidonic AcidsIn Vitro TechniquesBiologyGlyceridesProsencephalonInternal medicinemedicineAnimalsFuransGenes Immediate-EarlyEpilepsyCannabinoidsBrain-Derived Neurotrophic FactorExcitatory Postsynaptic PotentialsMice Inbred C57BLEndocrinologyGene Expression Regulationnervous systemchemistryMutationPyrazolesCannabinoidNeuroscienceEndocannabinoidsScience
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Cannabinoid modulation of hippocampal long-term memory is mediated by mTOR signaling.

2009

Cognitive impairment is one of the most important negative consequences associated with cannabis consumption. We found that CB1 cannabinoid receptor (CB1R) activation transiently modulated the mammalian target of rapamycin (mTOR)/p70S6K pathway and the protein synthesis machinery in the mouse hippocampus, which correlated with the amnesic properties of delta9-tetrahydrocannabinol (THC). In addition, non-amnesic doses of either the mTOR blocker rapamycin or the protein synthesis inhibitor anisomycin abrogated the amnesic-like effects of THC, pointing to a mechanism involving new protein synthesis. Moreover, using pharmacological and genetic tools, we found that THC long-term memory deficits …

MaleCannabinoid receptormedicine.medical_treatmentGlutamic AcidHippocampusReceptors N-Methyl-D-AspartateGlutamatergicchemistry.chemical_compoundMiceCognitionReceptor Cannabinoid CB1Memorymental disordersmedicineAnimalsDronabinolPI3K/AKT/mTOR pathwayAnisomycingamma-Aminobutyric AcidMice KnockoutNeuronsProtein Synthesis InhibitorsSirolimusMemory DisordersChemistryGeneral NeuroscienceTOR Serine-Threonine KinasesRibosomal Protein S6 Kinases 70-kDanervous systemKnockout mouseNMDA receptorPhosphorylationCannabinoidNeuroscienceProtein KinasesAnisomycinCentral Nervous System AgentsSignal TransductionNature neuroscience
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Effects of peroxisome proliferator-activated receptor alpha activation on pathways contributing to cholesterol homeostasis in rat hepatocytes

2004

International audience; Peroxisome proliferator-activated receptor alpha (PPARa) activation by fibrates controls expression of several genes involved in hepatic cholesterol metabolism. Other genes could be indirectly controlled in response to changes in cellular cholesterol availability. To further understand how fibrates may affect cholesterol synthesis, we investigated in parallel the changes in the metabolic pathways contributing to cholesterol homeostasis in liver. Ciprofibrate increased HMG-CoA reductase and FPP synthase mRNA levels in rat hepatocytes, together with cholesterogenesis from [14C] acetate and [3H] mevalonate. The up-regulation observed in fenofibrate- and WY-14,643-treate…

MaleCarboxy-Lyases[SDV]Life Sciences [q-bio]Receptors Cytoplasmic and NuclearAcetatesClofibric AcidMicechemistry.chemical_compound0302 clinical medicineMice KnockoutCarbon Isotopes0303 health sciencesFenofibrateFibric AcidsPeroxisomeUp-RegulationHMG-COA REDUCTASEDNA-Binding ProteinsCholesterolCHOLESTEROL METABOLISM030220 oncology & carcinogenesisHMG-CoA reductaseCholesteryl esterPeroxisome Proliferatorslipids (amino acids peptides and proteins)Peroxisome proliferator-activated receptor alphaSterol Regulatory Element Binding Protein 1Cell DivisionSignal Transductionmedicine.drugmedicine.medical_specialtyMevalonic AcidPeroxisome ProliferationBiologyCholesterol 7 alpha-hydroxylaseBile Acids and Salts03 medical and health sciencesInternal medicinemedicineAnimalsRNA MessengerMolecular Biology030304 developmental biologyCell BiologyRAT HEPATOCYTEPPARA-NULL MOUSERatsSterol regulatory element-binding proteinMice Inbred C57BLPyrimidinesEndocrinologychemistryFIBRATECCAAT-Enhancer-Binding ProteinsHepatocytesbiology.proteinHydroxymethylglutaryl CoA ReductasesTranscription Factors
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Classical Flt3L-dependent dendritic cells control immunity to protein vaccine

2014

DCs are critical for initiating immunity. The current paradigm in vaccine biology is that DCs migrating from peripheral tissue and classical lymphoid-resident DCs (cDCs) cooperate in the draining LNs to initiate priming and proliferation of T cells. Here, we observe subcutaneous immunity is Fms-like tyrosine kinase 3 ligand (Flt3L) dependent. Flt3L is rapidly secreted after immunization; Flt3 deletion reduces T cell responses by 50%. Flt3L enhances global T cell and humoral immunity as well as both the numbers and antigen capture capacity of migratory DCs (migDCs) and LN-resident cDCs. Surprisingly, however, we find immunity is controlled by cDCs and actively tempered in vivo by migDCs. Del…

MaleCellular immunityInjections IntradermalLangerinOvalbuminInjections SubcutaneousT cellImmunologyAntigen presentationGene ExpressionPriming (immunology)Mice Transgenicchemical and pharmacologic phenomenaLigandsInterferon-gammaMice03 medical and health sciences0302 clinical medicineAntigenT-Lymphocyte SubsetsImmunitymedicineAnimalsHumansImmunology and AllergyLectins C-Type030304 developmental biologyMice KnockoutAntigen PresentationVaccines0303 health sciencesbiologyMembrane ProteinsProteinsDendritic Cellsbiochemical phenomena metabolism and nutritionImmunity Humoral3. Good healthMice Inbred C57BLMannose-Binding Lectinsmedicine.anatomical_structureAntigens SurfaceHumoral immunityImmunologybiology.proteinbacteriaFemaleTranscription Factors030215 immunologyJournal of Experimental Medicine
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Mast cells as rapid innate sensors of cytomegalovirus by TLR3/TRIF signaling-dependent and -independent mechanisms

2014

The succinct metaphor, ‘the immune system's loaded gun', has been used to describe the role of mast cells (MCs) due to their storage of a wide range of potent pro-inflammatory and antimicrobial mediators in secretory granules that can be released almost instantly on demand to fight invaders. Located at host–environment boundaries and equipped with an arsenal of pattern recognition receptors, MCs are destined to be rapid innate sensors of pathogens penetrating endothelial and epithelial surfaces. Although the importance of MCs in antimicrobial and antiparasitic defense has long been appreciated, their role in raising the alarm against viral infections has been noted only recently. Work on cy…

MaleChemokineImmunologyCytomegalovirusBiologyCD8-Positive T-LymphocytesCCL5MiceImmune systemImmunology and AllergyCytotoxic T cellAnimalsMast CellsMice KnockoutIntegrasesMacrophagesDegranulationPattern recognition receptorhumanitiesToll-Like Receptor 3Killer Cells NaturalMice Inbred C57BLAdaptor Proteins Vesicular TransportInfectious DiseasesTRIFImmunologyTLR3Cytomegalovirus Infectionsbiology.proteinFemaleResearch Article
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Knockout of the KH-Type Splicing Regulatory Protein Drives Glomerulonephritis in MRL-Faslpr Mice

2021

KH-type splicing regulatory protein (KSRP) is an RNA-binding protein that promotes mRNA decay and thereby negatively regulates cytokine expression at the post-transcriptional level. Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by dysregulated cytokine expression causing multiple organ manifestations

MaleChemokineMice Inbred MRL lprQH301-705.5medicine.medical_treatmentLupus nephritisBiologyKidneyArticleImmune systemsystemic lupus erythematosusimmune system diseasesmedicinecytokineAnimalsCD11a AntigenRNA MessengerKSRPBiology (General)skin and connective tissue diseasesRegulation of gene expressionMice KnockoutSystemic lupus erythematosusFOXP3RNA-Binding ProteinsGlomerulonephritisGeneral Medicinemedicine.diseaseMice Inbred C57BLCytokineCancer researchbiology.proteinTrans-ActivatorsFemaleLymph NodesChemokinesBiomarkersglomerulonephritispost-transcriptional regulationCells
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Frontline: Interferon regulatory factor-1 as a protective gene in intestinal inflammation: role of TCRγ δ T cells and interleukin-18-binding protein

2004

The transcription factor IFN regulatory factor-1 (IRF-1) regulates production and activity of many inflammatory mediators and cells. Here, we investigated the role of IRF-1 in intestinal inflammation using clinical and histologic scores; inflammatory mediators were also measured in colonic tissue. Dextran sulfate sodium (DSS) or trinitrobenzene sulfonic acid (TNBS) was administered to wild-type (WT) or IRF-1 knockout (KO) mice. DSS or TNBS led to a dramatic increase in lethality and colitis severity in IRF-1 KO compared with WT mice. Reduced levels of IFN-γ and IL-18-binding protein (IL-18BP) were observed in the colon of IRF-1 KO mice, whereas levels of inducible nitric oxide synthase, cyc…

MaleChemokineT-LymphocytesImmunologyPopulationInterferon-gammaMicemedicineAnimalsImmunology and AllergyColitiseducationTranscription factorGlycoproteinsMice Knockouteducation.field_of_studybiologyT-cell receptorReceptors Antigen T-Cell gamma-deltaColitisPhosphoproteinsmedicine.diseaseMolecular biologyDNA-Binding ProteinsMice Inbred C57BLNitric oxide synthaseIRF1Immunologybiology.proteinIntercellular Signaling Peptides and ProteinsFemaleAntibodyInterferon Regulatory Factor-1European Journal of Immunology
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Toll-like receptor 5 deficiency exacerbates cardiac injury and inflammation induced by myocardial ischaemia-reperfusion in the mouse

2015

Myocardial ischaemia-reperfusion (MIR) triggers a sterile inflammatory response important for myocardial healing, but which may also contribute to adverse ventricular remodelling. Such inflammation is initiated by molecular danger signals released by damaged myocardium, which induce innate immune responses by activating toll-like receptors (TLRs). Detrimental roles have been recently reported for TLR2, TLR3 and TLR4. The role of other TLRs is unknown. We therefore evaluated the role of TLR5, expressed at high level in the heart, in the development of myocardial damage and inflammation acutely triggered by MIR. TLR5−/− and wild-type (WT) mice were exposed to MIR (30 min ischaemia, 2 h reperf…

MaleChemokinemedicine.medical_specialtyGenotypep38 mitogen-activated protein kinasesMyocardial InfarctionMyocardial Reperfusion InjuryInflammation030204 cardiovascular system & hematologyBiologyp38 Mitogen-Activated Protein KinasesVentricular Function LeftProinflammatory cytokineVentricular Dysfunction Left03 medical and health sciences0302 clinical medicine[SDV.MHEP.CSC]Life Sciences [q-bio]/Human health and pathology/Cardiology and cardiovascular systemInternal medicinemedicineAnimalsPhosphorylationProtein kinase B030304 developmental biologyInflammationMice Knockout0303 health sciencesToll-like receptorMyocardiumGeneral MedicineImmunity Innate3. Good healthMice Inbred C57BLDisease Models AnimalOxidative StressToll-Like Receptor 5CXCL2PhenotypeEndocrinologybiology.proteinTLR4Inflammation Mediatorsmedicine.symptomProto-Oncogene Proteins c-aktClinical Science
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Dppa3 expression is critical for generation of fully reprogrammed iPS cells and maintenance of Dlk1-Dio3 imprinting.

2014

Reprogramming of mouse somatic cells into induced pluripotent stem cells (iPSCs) often generates partially reprogrammed iPSCs (pre-iPSCs), low-grade chimera forming iPSCs (lg-iPSCs) and fully reprogrammed, high-grade chimera production competent iPSCs (hg-iPSCs). Lg-iPSC transcriptome analysis revealed misregulated Dlk1-Dio3 cluster gene expression and subsequently the imprinting defect at the Dlk1-Dio3 locus. Here, we show that germ-cell marker Dppa3 is present only in lg-iPSCs and hg-iPSCs, and that induction with exogenous Dppa3 enhances reprogramming kinetics, generating all hg-iPSCs, similar to vitamin C (Vc). Conversely, Dppa3-null fibroblasts show reprogramming block at pre-iPSCs sta…

MaleChromosomal Proteins Non-HistoneGreen Fluorescent ProteinsInduced Pluripotent Stem CellsMice TransgenicAscorbic AcidIodide PeroxidaseArticleGenomic ImprintingMiceAnimalsCrosses GeneticMice KnockoutGene Expression ProfilingCalcium-Binding ProteinsDNA MethylationFibroblastsMice Inbred C57BLRepressor ProteinsKineticsGerm CellsRetroviridaeGene Expression RegulationIntercellular Signaling Peptides and ProteinsFemaleProtein BindingNature communications
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