Search results for "Knockout"

showing 10 items of 806 documents

Differential cystine and dibasic amino acid handling after loss of function of the amino acid transporter b0,+ AT (Slc7a9) in mice

2013

Cystinuria is an autosomal recessive disease caused by mutations in SLC3A1 ( rBAT) and SLC7A9 ( b 0,+ AT). Gene targeting of the catalytic subunit ( Slc7a9) in mice leads to excessive excretion of cystine, lysine, arginine, and ornithine. Here, we studied this non-type I cystinuria mouse model using gene expression analysis, Western blotting, clearance, and brush-border membrane vesicle (BBMV) uptake experiments to further characterize the renal and intestinal consequences of losing Slc7a9 function. The electrogenic and BBMV flux studies in the intestine suggested that arginine and ornithine are transported via other routes apart from system b0,+. No remarkable gene expression changes were…

Malemedicine.medical_specialtyPeptide transporterArgininePhysiologyLysineCystineSLC7A9BiologyKidneyGFRMicechemistry.chemical_compoundInternal medicinemedicineAnimalsAmino acid transporterMice Knockoutchemistry.chemical_classificationKidneyCystinuriaAmino Acids DiaminoCystinuriaOrnithinemedicine.diseaseAmino acidMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureEndocrinologychemistryBiochemistryAmino Acid Transport Systems BasicCystineGlomerular Filtration Rate
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Paracrine Activation of Hepatic CB1 Receptors by Stellate Cell-Derived Endocannabinoids Mediates Alcoholic Fatty Liver

2008

SummaryAlcohol-induced fatty liver, a major cause of morbidity, has been attributed to enhanced hepatic lipogenesis and decreased fat clearance of unknown mechanism. Here we report that the steatosis induced in mice by a low-fat, liquid ethanol diet is attenuated by concurrent blockade of cannabinoid CB1 receptors. Global or hepatocyte-specific CB1 knockout mice are resistant to ethanol-induced steatosis and increases in lipogenic gene expression and have increased carnitine palmitoyltransferase 1 activity, which, unlike in controls, is not reduced by ethanol treatment. Ethanol feeding increases the hepatic expression of CB1 receptors and upregulates the endocannabinoid 2-arachidonoylglycer…

Malemedicine.medical_specialtyPhysiologyHUMDISEASEArachidonic AcidsGlyceridesMiceCarnitine palmitoyltransferase 1PiperidinesReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsParacrine CommunicationmedicineAnimalsReceptorDiet Fat-RestrictedMolecular BiologyCells CulturedMice KnockoutCarnitine O-PalmitoyltransferaseEthanolChemistryLipogenesisFatty AcidsFatty liverCell Biologymedicine.diseaseEndocannabinoid systemCoculture TechniquesUp-RegulationMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologyLiverLipogenesisHepatocytesHepatic stellate cellPyrazoleslipids (amino acids peptides and proteins)Alcoholic fatty liverFatty Acid SynthasesRimonabantSteatosisSterol Regulatory Element Binding Protein 1Oxidation-ReductionEndocannabinoidsFatty Liver AlcoholicCell Metabolism
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Alterations in the Hippocampal Endocannabinoid System in Diet-Induced Obese Mice

2010

The endocannabinoid (eCB) system plays central roles in the regulation of food intake and energy expenditure. Its alteration in activity contributes to the development and maintenance of obesity. Stimulation of the cannabinoid receptor type 1 (CB1receptor) increases feeding, enhances reward aspects of eating, and promotes lipogenesis, whereas its blockade decreases appetite, sustains weight loss, increases insulin sensitivity, and alleviates dysregulation of lipid metabolism. The hypothesis has been put forward that the eCB system is overactive in obesity. Hippocampal circuits are not directly involved in the neuronal control of food intake and appetite, but they play important roles in hed…

Malemedicine.medical_specialtyPolyunsaturated Alkamidesmedicine.medical_treatmentmedia_common.quotation_subjectArachidonic AcidsBiologyHippocampusArticlegamma-Aminobutyric acidGlyceridesMice03 medical and health sciences0302 clinical medicineReceptor Cannabinoid CB1Internal medicineCannabinoid Receptor ModulatorsCannabinoid receptor type 1medicineAnimalsObesityReceptorgamma-Aminobutyric Acid030304 developmental biologymedia_commonMice KnockoutNeurons0303 health sciencesLong-Term Synaptic DepressionGeneral NeuroscienceAppetiteDietary FatsEndocannabinoid systemMice Inbred C57BLDisease Models AnimalLipoprotein LipaseEndocrinologynervous systemSynapsesSynaptic plasticitylipids (amino acids peptides and proteins)CannabinoidDiet-induced obese030217 neurology & neurosurgeryEndocannabinoidsmedicine.drugThe Journal of Neuroscience
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Adenosine A2A receptors in diffuse dermal fibrosis: pathogenic role in human dermal fibroblasts and in a murine model of scleroderma.

2006

Objective Adenosine regulates inflammation and tissue repair, and adenosine A2A receptors promote wound healing by stimulating collagen matrix production. We therefore examined whether adenosine A2A receptors contribute to the pathogenesis of dermal fibrosis. Methods Collagen production by primary human dermal fibroblasts was analyzed by real-time polymerase chain reaction, 14C-proline incorporation, and Sircol assay. Intracellular signaling for dermal collagen production was investigated using inhibitors of MEK-1 and by demonstration of ERK phosphorylation. In vivo effects were studied in a bleomycin-induced dermal fibrosis model using adenosine A2A receptor–deficient wild-type littermate …

Malemedicine.medical_specialtyReceptor Adenosine A2AImmunologyMAP Kinase Kinase 1Adenosine A2A receptorGene ExpressionBiologyMiceRheumatologyFibrosisInternal medicinemedicineImmunology and AllergyAnimalsHumansPharmacology (medical)RNA MessengerEnzyme InhibitorsReceptorCells CulturedMice Knockoutintegumentary systemTriazinesDermisPurinergic signallingFibroblastsTriazolesAdenosine A3 receptormedicine.diseaseAdenosineAdenosine receptorFibrosisMice Inbred C57BLDisease Models AnimalHydroxyprolineEndocrinologyScleroderma DiffuseCancer researchCollagenWound healingmedicine.drugArthritis and rheumatism
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Molecular and functional interactions between tumor necrosis factor-alpha receptors and the glutamatergic system in the mouse hippocampus: Implicatio…

2009

Tumor necrosis factor (TNF)-alpha is a proinflammatory cytokine acting on two distinct receptor subtypes, namely p55 and p75 receptors. TNF-alpha p55 and p75 receptor knockout mice were previously shown to display a decreased or enhanced susceptibility to seizures, respectively, suggesting intrinsic modifications in neuronal excitability. We investigated whether alterations in glutamate system function occur in these naive knockout mice with perturbed cytokine signaling that could explain their different propensity to develop seizures. Using Western blot analysis of hippocampal homogenates, we found that p55(-/-) mice have decreased levels of membrane GluR3 and NR1 glutamate receptor subuni…

Malemedicine.medical_specialtyReceptors Kainic acidMicrodialysisAction PotentialsGlutamic AcidKainate receptorAMPA receptorIn Vitro TechniquesBiologyHippocampusReceptors N-Methyl-D-Aspartateelectrophysiology microiontophoresisSettore BIO/09 - FisiologiaMicechemistry.chemical_compoundGlutamatergicReceptors Kainic AcidSeizuresInternal medicinemedicineAnimalsReceptors Tumor Necrosis Factor Type IIReceptors AMPAMice KnockoutNeuronsInflammationTumor Necrosis Factor-alphaGeneral NeuroscienceGlutamate receptorProtein SubunitsEndocrinologymedicine.anatomical_structureReceptors Glutamatenervous systemchemistryReceptors Tumor Necrosis Factor Type IMetabotropic glutamate receptorAstrocytesCytokinesNMDA receptorNBQXDisease SusceptibilityAstrocyte
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Melatonin signaling modulates clock genes expression in the mouse retina.

2014

Previous studies have shown that retinal melatonin plays an important role in the regulation of retinal daily and circadian rhythms. Melatonin exerts its influence by binding to G-protein coupled receptors named melatonin receptor type 1 and type 2 and both receptors are present in the mouse retina. Earlier studies have shown that clock genes are rhythmically expressed in the mouse retina and melatonin signaling may be implicated in the modulation of clock gene expression in this tissue. In this study we determined the daily and circadian expression patterns of Per1, Per2, Bmal1, Dbp, Nampt and c-fos in the retina and in the photoreceptor layer (using laser capture microdissection) in C3H-f…

Malemedicine.medical_specialtyendocrine systemgenetic structuresOcular AnatomyReceptors Melatoninlcsh:MedicineBiologyMelatonin receptorBiochemistryRetinaPinealocyteMelatoninGene Knockout TechniquesMiceOcular SystemInternal medicinemedicineAnimalsPhotoreceptor Cellslcsh:ScienceMolecular BiologyMelatoninRetinaMultidisciplinarylcsh:RBiology and Life SciencesCell biologyCircadian RhythmCLOCKPER2Circadian OscillatorsCircadian Rhythmsmedicine.anatomical_structureEndocrinologyGene Expression RegulationDaylightFemalelcsh:Qsense organsSignal transductionAnatomyChronobiologyhormones hormone substitutes and hormone antagonistsmedicine.drugPER1Research ArticleSignal TransductionPLoS ONE
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A non-redundant role for OX40 in the competitive fitness of Treg in response to IL-2.

2010

OX40 stimulation is known to enhance activation of effector T cells and to inhibit induction and suppressive function of Treg. Here we uncovered a novel role of OX40 in sustaining Treg competitive fitness in vivo, during repopulation of lymphopenic hosts and reconstitution of BM chimeras. Defective expansion of OX40-null Treg diminished their ability to suppress inflammation in a model of lymphopenia-driven colitis. OX40-mediated promotion of Treg fitness spanned beyond lymphopenic environments, as endogenous Treg in OX40-null mice showed decreased accumulation during thymic development, enhanced susceptibility to antibody-mediated depletion and defective turnover following thymectomy. In v…

Malemedicine.medical_treatmentImmunologyBlotting Westernchemical and pharmacologic phenomenaEndogenyInflammationSuppressor of Cytokine Signaling ProteinsT-Lymphocytes RegulatoryMiceSuppressor of Cytokine Signaling 1 ProteinLymphopeniaOX40; Treg; IL-2.medicineSTAT5 Transcription FactorImmunology and AllergyAnimalsOX40PhosphorylationReceptorSTAT5Cell ProliferationMice KnockoutbiologyEffectorCell growthSuppressor of cytokine signaling 1hemic and immune systemsReceptors OX40IL-2.ColitisFlow Cytometrycytokinescompetitive fitnessSpecific Pathogen-Free OrganismsThymectomyMice Inbred C57BLTregRadiation ChimeraImmunologybiology.proteinInterleukin-2costimulatory moleculesmedicine.symptomcompetitive fitness; costimulatory molecules; cytokines; treg
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Reconstitution of the Complement Function in C1q-Deficient (C1qa−/−) Mice with Wild-Type Bone Marrow Cells

2001

Abstract Besides Ab-independent and Ab-dependent activation of the complement classical pathway in host defense, C1q plays a key role in the processing of immune complexes and in the clearance of apoptotic cells. In humans, C1q deficiency leads to systemic lupus erythematosus-like symptoms in over 90% of the cases, thus making this defect a strong disease susceptibility factor. Similarly, C1q-deficient mice (C1qa−/−) develop systemic lupus erythematosus-like symptoms, such as autoantibodies and glomerulonephritis. We have previously provided evidence that C1q is produced by cells of the monocyte-macrophage lineage. In this study, we have tested whether transplantation of bone marrow cells w…

Malemedicine.medical_treatmentImmunologychemical and pharmacologic phenomenaHematopoietic stem cell transplantationBiologyMiceClassical complement pathwayImmune systemimmune system diseasesY ChromosomemedicineAnimalsLupus Erythematosus SystemicImmunology and AllergyTissue DistributionRNA Messengerskin and connective tissue diseasesBone Marrow TransplantationMice KnockoutLupus erythematosusComplement C1qHematopoietic Stem Cell TransplantationGlomerulonephritismedicine.diseaseMice Inbred C57BLTransplantationKineticsmedicine.anatomical_structureImmunologyFemaleBone marrowStem cellThe Journal of Immunology
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Toll-like receptor 2 mediates prostaglandin E2 production in murine peritoneal macrophages and splenocytes in response to Candida albicans

2004

The involvement of Toll-like receptor 2 (TLR2) and TLR4 in triggering signal transduction pathways leading to prostaglandin E(2) (PGE(2)) production in response to Candida albicans has been studied in cells from wild-type, TLR2-/- and TLR4-/- knockout mice. In vitro PGE(2) production by macrophages challenged with zymosan, yeast or hypha cells was strongly inhibited in TLR2-deficient cells, but not in TLR4-/- cells, as compared to macrophages from wild-type mice. PGE(2) production was dependent on de novo cyclooxygenase-2 (Cox2) synthesis, since unchallenged cells failed to produce PGE(2) and specific Cox2 inhibition during challenge totally blocked PGE(2) production. Similar results were o…

Malemedicine.medical_treatmentReceptors Cell SurfaceBiologyMicrobiologyDinoprostoneMicechemistry.chemical_compoundCandida albicansmedicineAnimalsProstaglandin E2Candida albicansMolecular BiologyCells CulturedMice KnockoutToll-like receptorZymosanGeneral Medicinebiology.organism_classificationMolecular biologyToll-Like Receptor 2Corpus albicansToll-Like Receptor 4TLR2chemistryCyclooxygenase 2Prostaglandin-Endoperoxide SynthasesImmunologyMacrophages PeritonealTLR4Femalelipids (amino acids peptides and proteins)Signal Transductionmedicine.drugProstaglandin EResearch in Microbiology
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Targeting transcription factor Stat4 uncovers a role for interleukin-18 in the pathogenesis of severe lupus nephritis in mice

2011

Polymorphisms in the transcription factor Stat4 gene have been implicated as risk factors for systemic lupus erythematosus. Although some polymorphisms have a strong association with autoantibodies and nephritis, their impact on pathophysiology is still unknown. To explore this further we used signal transducers and activators of transcription 4 (Stat4) knockout MRL/MpJ-Fas(lpr)/Fas(lpr) (MRL-Fas(lpr)) mice and found that they did not differ in survival or renal function from Stat4-intact MRL-Fas(lpr) mice. Circulating interleukin (IL)-18 levels, however, were elevated in Stat4-deficient compared to Stat4-intact mice, suggesting that this interleukin might contribute to the progression of l…

Malemusculoskeletal diseasesMice Inbred MRL lprchronic inflammationLupus nephritisKidneyInterleukin-23ArticleProinflammatory cytokineOligodeoxyribonucleotides AntisenseGene Knockout TechniquesInterferon-gammaMiceimmune system diseasesmedicineAnimalsskin and connective tissue diseasesSTAT4DNA PrimersAutoimmune diseaseMice Knockoutlupus nephritisMice Inbred BALB CBase Sequencebusiness.industryGene Transfer TechniquesInterleukin-18InterleukinGlomerulonephritishemic and immune systemsSTAT4 Transcription Factormedicine.diseaseInterleukin-12chronic glomerulonephritisNephrologyImmunologyInterleukin 18FemalebusinessNephritisKidney International
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