Search results for "Knockout"

showing 10 items of 806 documents

CB1 cannabinoid receptor-mediated aggressive behavior

2013

This study examined the role of cannabinoid CB1 receptors (CB1r) in aggressive behavior. Social encounters took place in grouped and isolated mice lacking CB1r (CB1KO) and in wild-type (WT) littermates. Cognitive impulsivity was evaluated in the delayed reinforcement task (DRT). Gene expression analyses of monoaminooxidase-A (MAO-A), catechol-o-methyl-transferase (COMT), 5-hydroxytriptamine transporter (5-HTT) and 5-HT1B serotonergic receptor (5HT1Br) in the median and dorsal raphe nuclei (MnR and DR, respectively) and in the amygdala (AMY) were performed by real time-PCR. Double immunohistochemistry studies evaluated COMT and CB1r co-localization in the raphe nuclei and in the cortical (AC…

AgonistMalemedicine.medical_specialtyCannabinoid receptorTime Factorsmedicine.drug_classmedicine.medical_treatmentPoison controlArachidonic AcidsSerotonergicCatechol O-MethyltransferaseAmygdalaCellular and Molecular NeuroscienceMiceDorsal raphe nucleusReceptor Cannabinoid CB1Internal medicinemedicineAnimalsInterpersonal RelationsMonoamine OxidasePharmacologyCannabinoid Receptor AgonistsMice KnockoutSerotonin Plasma Membrane Transport ProteinsAmygdalaSurgeryAggressionmedicine.anatomical_structureEndocrinologynervous systemGene Expression RegulationImpulsive BehaviorReceptor Serotonin 5-HT1BConditioning OperantRaphe NucleiCannabinoidRaphe nucleiPsychologyReinforcement Psychology
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Methylprednisolone prevents nerve injury-induced hyperalgesia in neprilysin knockout mice.

2013

The pathophysiology of the complex regional pain syndrome involves enhanced neurogenic inflammation mediated by neuropeptides. Neutral endopeptidase (neprilysin, NEP) is a key enzyme in neuropeptide catabolism. Our previous work revealed that NEP knock out (ko) mice develop more severe hypersensitivity to thermal and mechanical stimuli after chronic constriction injury (CCI) of the sciatic nerve than wild-type (wt) mice. Because treatment with glucocorticoids is effective in early complex regional pain syndrome, we investigated whether methylprednisolone (MP) reduces pain and sciatic nerve neuropeptide content in NEP ko and wt mice with nerve injury. After CCI, NEP ko mice developed more se…

Agonistmedicine.medical_specialtymedicine.drug_classNeuropeptideSubstance PMethylprednisolonechemistry.chemical_compoundMiceInternal medicineMedicineAnimalsNeprilysinMice KnockoutNeurogenic inflammationbusiness.industryfungiNerve injuryMice Inbred C57BLAnesthesiology and Pain MedicineEndocrinologyNeuroprotective AgentsNeurologychemistryHyperalgesiaAnesthesiaHyperalgesiaNeprilysinNeurology (clinical)Sciatic nervemedicine.symptomSciatic NeuropathybusinessPainReferences
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Altered atypical coupling of γ-aminobutyrate type A receptor agonist and convulsant binding sites in subunit-deficient mouse lines

2001

We searched for subunit correlations for GABA(A) receptor-associated atypically GABA-insensitive [35S]TBPS binding. The homomeric beta3 subunit receptors could be excluded, as GABA-insensitive [35S]TBPS binding was present in beta3-/- mice. Localization of GABA-insensitive [35S]TBPS binding correlated best with those of delta, alpha4 and alpha6 subunit mRNAs. The amounts of GABA-insensitive [35S]TBPS binding components were increased in delta-/- mice, but dramatically reduced in alpha6-/- mice, suggesting a role for alpha6 but excluding delta subunits.

Agonistmedicine.medical_specialtymedicine.drug_classProtein subunitMolecular Sequence DataConvulsantsBiologySulfur Radioisotopesmedicine.disease_causeMiceRadioligand AssayCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsHomomericRNA MessengerBinding siteReceptorGABA AgonistsMolecular BiologyBrain ChemistryMice KnockoutMutationBinding SitesGABAA receptorBridged Bicyclo Compounds HeterocyclicReceptors GABA-AMolecular biologyEndocrinologynervous systemConvulsantMolecular Brain Research
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Assessment of mechanisms driving non-linear dose-response relationships in genotoxicity testing.

2014

In genetic toxicology, risk assessment has traditionally adopted linear dose-responses for any compound that causes genotoxic effects. Increasing evidence of non-linear dose-responses, however, suggests potential cellular tolerance to low levels of many genotoxicants with diverse modes of action. Such putative non-linear dose-responses need to be substantiated by strong mechanistic data that identifies the mechanisms responsible for the tolerance to low doses. This can be achieved by experimental demonstration of cytoprotective mechanisms and by providing experimental support for the existence of tolerance mechanisms against low dose effects. By highlighting key experiments into low dose me…

Alkylating AgentsDNA repairmedicine.drug_classTopoisomerase InhibitorsHealth Toxicology and MutagenesisTransgeneComputational biologyBiologyRisk AssessmentGenotoxicity testingToxicologyGeneticsmedicineAnimalsHumansGene knockoutDose-Response Relationship DrugMutagenicity TestsLow doseNucleosidesAneugensOxidantsModels ChemicalParticulate MatterTopoisomerase inhibitorGenetic ToxicologyDNA DamageMutagensMutation research. Reviews in mutation research
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Primary mouse fibroblasts deficient for c-Fos, p53 or for both proteins are hypersensitive to UV light and alkylating agent-induced chromosomal break…

2000

The important regulatory proteins, c-Fos and p53 are induced by exposure of cells to a variety of DNA damaging agents. To investigate their role in cellular defense against genotoxic compounds, we comparatively analysed chromosomal aberrations and apoptosis induced by ultraviolet (UV-C) light and the potent alkylating agent methyl methanesulfonate (MMS) in primary diploid mouse fibroblasts knockout for either c-Fos or p53, or double knockout for both genes. We show that c-Fos and p53 deficient fibroblasts are more sensitive than the corresponding wild-type cells as to the induction of chromosomal aberrations and apoptosis. Double knockout fibroblasts lacking both c-Fos and p53 are viable an…

Alkylating AgentsUltraviolet RaysDNA repairDNA damageHealth Toxicology and MutagenesisDrug ResistanceMutagenesis (molecular biology technique)ApoptosisBiologyRadiation ToleranceCell LineMicechemistry.chemical_compoundGeneticsAnimalsMolecular BiologyGene knockoutChromosome AberrationsMice KnockoutGenes fosFibroblastsCell cycleGenes p53Molecular biologyMethyl methanesulfonatechemistryApoptosisCell cultureTumor Suppressor Protein p53Proto-Oncogene Proteins c-fosDNA DamageMutation Research/Fundamental and Molecular Mechanisms of Mutagenesis
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Interruption of CD28-mediated costimulation during allergen challenge protects mice from allergic airway disease

2012

Background Allergic asthma is a T H 2-promoted hyperreactivity with an immediate, IgE, and mast cell–dependent response followed by eosinophil-dominated inflammation and airway obstruction. Objective Because costimulation by CD28 is essential for T H 2 but not T H 1 responses, we investigated the effect of selective interference with this pathway in mice using the models of ovalbumin and house dust mite–induced airway inflammation. Methods To study the role of CD28 in the effector phase of allergic airway inflammation, we developed an inducibly CD28-deleting mouse strain or alternatively used a CD28 ligand-binding site–specific mouse anti-mouse mAb blocking CD28 engagement. Results We show …

Allergic asthmaLymphocyte ActivationImmunoglobulin Emedicine.disease_causeT-Lymphocytes RegulatoryMice0302 clinical medicineAirway resistanceAllergenImmunology and AllergySensitizationMice Inbred BALB C0303 health sciencesbiologyAntibodies Monoclonalovalbuminrespiratory system3. Good healthmedicine.anatomical_structurecostimulationconditional CD28 knockout miceFemalemedicine.symptomImmunologyInflammation03 medical and health sciencesTh2 CellsCD28 AntigensRespiratory HypersensitivitymedicineAnimalsHumansAntigens DermatophagoidesLymphocyte CountAntibodies Blocking030304 developmental biologyHouse dust miteCD28-specific mAbbusiness.industryReceptor Cross-TalkAirway obstructionmedicine.diseasebiology.organism_classificationMice Mutant Strainsrespiratory tract diseasesDisease Models AnimalCTLA-4Immunologybiology.proteinbusiness030215 immunology
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Technical advance: Soluble OX40 molecule mimics regulatory T cell modulatory activity on FCεRI-dependent mast cell degranulation

2011

ABSTRACT Tregs play a central role in modulating FcɛRI-dependent MC effector functions in the course of the allergic response. Cellular interaction depends on the constitutive expression of OX40 on Tregs and the OX40L counterpart on MCs. Study of OX40L signaling on MCs is hampered by the need of a highly purified molecule, which triggers OX40L specifically. We now report that sOX40 mimics the physiological activity of Treg interaction by binding to activated MCs. When treated with sOX40, activated MCs showed decreased degranulation and Ca++ influx, whereas PLC-γ2 phosphorylation remained unaffected. Once injected into experimental animals, sOX40 not only located within the endothelium but a…

AllergyCell DegranulationRegulatory T cellImmunologyOX40 LigandAllergy; Cell activation; CostimulationBiologymedicine.disease_causeT-Lymphocytes RegulatoryCell DegranulationMiceHypersensitivitymedicineAnimalsImmunology and AllergyMast CellsPhosphorylationReceptorCell activationMice KnockoutMembrane GlycoproteinsPhospholipase C gammaReceptors IgEDegranulationCell BiologyReceptors OX40humanitiesCell biologymedicine.anatomical_structureCostimulationTechnical AdvanceSolubilityTumor Necrosis FactorsAllergic responsePhosphorylationSignal transductionCell activation
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T cell killing by tolerogenic dendritic cells protects mice from allergy.

2011

It is well established that allergy development can be prevented by repeated low-dose exposure to contact allergens. Exactly which immune mechanisms are responsible for this so-called low zone tolerance (LZT) is not clear, although CD8⁺ suppressor T cells are known to have a role. Here, we show that TNF released by tolerogenic CD11⁺CD8⁺ DCs located in skin-draining lymph nodes is required and sufficient for development of tolerance to contact allergens in mice. DC-derived TNF protected mice from contact allergy by inducing apoptosis in allergen-specific effector CD8⁺ T cells via TNF receptor 2 but did not contribute to the generation and function of the regulatory T cells associated with LZ…

AllergyT cellApoptosisBiologyCD8-Positive T-LymphocytesDermatitis Contactlaw.inventionImmune toleranceMicelawmedicineHypersensitivityImmune ToleranceAnimalsReceptors Tumor Necrosis Factor Type IIReceptorMice KnockoutEffectorTumor Necrosis Factor-alphaGeneral MedicineDendritic CellsAllergensmedicine.diseaseMice Inbred C57BLmedicine.anatomical_structureApoptosisReceptors Tumor Necrosis Factor Type IImmunologySuppressorTumor necrosis factor alphaThe Journal of clinical investigation
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Effective treatment of allergic airway inflammation with Helicobacter pylori immunomodulators requires BATF3-dependent dendritic cells and IL-10

2014

The prevalence of allergic asthma and other atopic diseases has reached epidemic proportions in large parts of the developed world. The gradual loss of the human indigenous microbiota has been held responsible for this trend. The bacterial pathogen Helicobacter pylori is a constituent of the normal gastric microbiota whose presence has been inversely linked to allergy and asthma in humans and experimental models. Here we show that oral or i.p. tolerization with H. pylori extract prevents the airway hyperresponsiveness, bronchoalveolar eosinophilia, pulmonary inflammation, and Th2 cytokine production that are hallmarks of allergen-induced asthma in mice. Asthma protection is not conferred by…

Allergybacterial persistence determinantsT-Lymphocytes Regulatorybacterial immunomodulationImmune toleranceMiceBacterial ProteinsImmune TolerancemedicineAnimalsHumansImmunologic FactorsEosinophiliaAsthmaMice KnockoutAntigens Bacterial1000 MultidisciplinaryMultidisciplinaryHelicobacter pyloribiologyallergy and asthma prevention10061 Institute of Molecular Cancer ResearchInterleukin-18tolerogenic dendritic cellsDendritic Cellsgamma-GlutamyltransferaseDendritic cellBiological SciencesAllergensHelicobacter pyloribacterial infections and mycosesmedicine.diseasebiology.organism_classificationAsthmaInterleukin-10respiratory tract diseases3. Good healthMice Inbred C57BLRepressor ProteinsDisease Models AnimalInterleukin 10Basic-Leucine Zipper Transcription FactorsImmunology570 Life sciences; biologyInterleukin 18medicine.symptom
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Stressor-related impairment of synaptic transmission in hippocampal slices from α-synuclein knockout mice

2004

The role of alpha-synuclein (alpha-Syn) has recently received considerable attention because it seems to play a role in Parkinson's disease (PD). Missense mutations in the alpha-Syn gene were found in autosomal dominant PD and alpha-Syn was shown to be a major constituent of protein aggregates in sporadic PD and other synucleinopathies. Under normal conditions, alpha-Syn protein is found exclusively in synaptic terminals. However, the potential participation of alpha-synuclein in maintaining and regulating synaptic efficacy is unknown. We have investigated the excitatory synaptic modulation of alpha-synuclein in CA1 pyramidal neurons, using the in vitro hippocampal slice technique. The 4-am…

Alpha-synucleinanimal diseasesGeneral NeuroscienceHippocampusNeurotransmissionBiologynervous system diseaseschemistry.chemical_compoundSynaptic fatiguenervous systemchemistrySynaptic augmentationSynaptic plasticityKnockout mouseExcitatory postsynaptic potentialNeuroscienceEuropean Journal of Neuroscience
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