Search results for " Knockout"

showing 10 items of 764 documents

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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Human Oxidation-Specific Antibodies Reduce Foam Cell Formation and Atherosclerosis Progression

2011

ObjectivesWe sought to assess the in vivo importance of scavenger receptor (SR)–mediated uptake of oxidized low-density lipoprotein (OxLDL) in atherogenesis and to test the efficacy of human antibody IK17-Fab or IK17 single-chain Fv fragment (IK17-scFv), which lacks immunologic properties of intact antibodies other than the ability to inhibit uptake of OxLDL by macrophages, to inhibit atherosclerosis.BackgroundThe unregulated uptake of OxLDL by macrophage SR contributes to foam cell formation, but the importance of this pathway in vivo is uncertain.MethodsCholesterol-fed low-density lipoprotein receptor knockout (LDLR−/−) mice were treated with intraperitoneal infusion of human IK17-Fab (2.…

MaleoxidationGenetic enhancementGreen Fluorescent Proteins030204 cardiovascular system & hematologymedicine.disease_causeArticleAdenoviridaeMice03 medical and health sciences0302 clinical medicineIn vivoAnimalsHumansantibodiesMedicineScavenger receptorReceptorImmunoglobulin Fragments030304 developmental biologyFoam cellHomeodomain ProteinsMice Knockout0303 health sciencesbiologybusiness.industryMacrophagesscavenger receptorsgene therapyRecombinant Proteins3. Good healthLipoproteins LDLMice Inbred C57BLAdenoviridaeReceptors LDLImmunologyDisease ProgressionCancer researchbiology.proteinlipids (amino acids peptides and proteins)atherosclerosisAntibodyCardiology and Cardiovascular MedicinebusinessFoam CellsLipoproteinJournal of the American College of Cardiology
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Rac1 GTPase, a multifunctional player in the regulation of genotoxic stress response

2013

The Ras-related C3 botulinum toxin substrate 1 (Rac1) belongs to the Ras-homologous (Rho) family of small GTPases, which transduce signals from the outside to the inside of a cell. Rac1 becomes activated upon ligand binding of a variety of receptors, including receptor tyrosine kinases and heterotrimeric G-protein-coupled receptors. After GTP loading by guanine exchange factors (GEFs), GTP-bound Rac1 engages numerous effector proteins, thereby eventually regulating cell motility and adhesion, cell cycle progression through G1, mitosis and meiosis, as well as cell death and metastasis.1 Besides, Rac1 adjusts cellular responses to genotoxic agents, such as UV light and alkylating agents, by r…

Malerac1 GTP-Binding Proteintopoisomerase IIAgingRHOADNA repairDNA damagep38 mitogen-activated protein kinasesApoptosisRAC1Editorials: Cell Cycle FeaturesDNA damage responseReceptor tyrosine kinasechemical carcinogenesisHistonesMiceTransforming Growth Factor betaRho GTPasesAnimalsMolecular BiologyTranscription factoranthracyclinesMice KnockoutbiologyKinaseNeuropeptidesConnective Tissue Growth FactorHMG-CoA reductase inhibitors (statins)Cell BiologyFibrosisgenotoxic stressActinsrac GTP-Binding ProteinsCell biologyOxidative Stressnormal tissue damageGene Expression RegulationLiverBiochemistryDoxorubicinGamma Raysbiology.proteinFemaleDNA DamageMutagensSignal TransductionDevelopmental BiologyCell Cycle
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Involvement of plasmalogens in post-natal retinal vascular development

2014

Objective: Proper development of retinal blood vessels is essential to ensure sufficient oxygen and nutrient supplies to the retina. It was shown that polyunsaturated fatty acids (PUFAs) could modulate factors involved in tissue vascularization. A congenital deficiency in ether-phospholipids, also termed "plasmalogens'', was shown to lead to abnormal ocular vascularization. Because plasmalogens are considered to be reservoirs of PUFAs, we wished to improve our understanding of the mechanisms by which plasmalogens regulate retinal vascular development and whether the release of PUFAs by calcium-independent phospholipase A2 (iPLA2) could be involved. [br/] Methods and Results: By characterizi…

MaleretinaOrganes des sensAngiogenesis[ SDV.AEN ] Life Sciences [q-bio]/Food and Nutritionlcsh:MedicineRetinal NeovascularizationBiochemistryImmunoenzyme TechniquesMicechemistry.chemical_compoundangiogenesisMedicine and Health Sciencesangiogenesis;astrocytes;capillaries;endothelial cells;gene expression;phospholipids;retina;retinal vesselscapillarieslcsh:ScienceCells CulturedOligonucleotide Array Sequence AnalysisMice KnockoutMultidisciplinarymedicine.diagnostic_testReverse Transcriptase Polymerase Chain ReactionLipidsendothelial cellsCell biologyEndothelial stem cellmedicine.anatomical_structureBiochemistry[ SDV.MHEP.OS ] Life Sciences [q-bio]/Human health and pathology/Sensory OrgansAlimentation et NutritionFatty Acids UnsaturatedRetinal DisordersFemaleResearch ArticleAstrocyteEndotheliumSensory OrgansPlasmalogensBiologyReal-Time Polymerase Chain ReactionGroup VI Phospholipases A2AngiopoietinElectroretinographymedicineFood and NutritionAnimalsRNA Messenger[SDV.MHEP.OS]Life Sciences [q-bio]/Human health and pathology/Sensory OrgansphospholipidsRetinaGene Expression Profilinglcsh:Rretinal vesselsastrocytesBiology and Life SciencesRetinalMice Inbred C57BLOphthalmologyAnimals Newbornchemistrygene expressionlcsh:QEndothelium Vascular[SDV.AEN]Life Sciences [q-bio]/Food and NutritionAcyltransferasesBiomarkersDevelopmental BiologyElectroretinography
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Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independen…

2011

OBJECTIVE: Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein. METHODS AND RESULTS: Immunoblotting studies revealed a marked reduction in p27-phospho-Ser10 in atheroscleroti…

Malerho GTP-Binding ProteinsRHOAMoesinMiceApolipoproteins ERadixinSerinemedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein kinase ACell ProliferationFoam cellMice Knockoutrho-Associated KinasesbiologyArteriesAtherosclerosismedicine.diseaseCell biologyMice Inbred C57BLDisease Models AnimalAtheromaCase-Control StudiesImmunologyDisease Progressionbiology.proteinPhosphorylationFemalerhoA GTP-Binding ProteinCardiology and Cardiovascular MedicineCyclin-Dependent Kinase Inhibitor p27Foam CellsSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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Metalloproteases meprin α and meprin β are C- and N-procollagen proteinases important for collagen assembly and tensile strength.

2013

Type I fibrillar collagen is the most abundant protein in the human body, crucial for the formation and strength of bones, skin, and tendon. Proteolytic enzymes are essential for initiation of the assembly of collagen fibrils by cleaving off the propeptides. We report that Mep1a −/− and Mep1b −/− mice revealed lower amounts of mature collagen I compared with WT mice and exhibited significantly reduced collagen deposition in skin, along with markedly decreased tissue tensile strength. While exploring the mechanism of this phenotype, we found that cleavage of full-length human procollagen I heterotrimers by either meprin α or meprin β led to the generation of mature collagen molecules that s…

Materials scienceConnective tissueCHO CellsCollagen Type IMiceCricetulusFibrosisCricetinaeTensile StrengthmedicineAnimalsHumansProtein precursorSkinMice KnockoutMetalloproteinaseMultidisciplinaryProteolytic enzymesMetalloendopeptidasesProcollagen N-EndopeptidaseBiological Sciencesmedicine.diseaseCell biologyProcollagen peptidaseCollagen type I alpha 1medicine.anatomical_structureHEK293 CellsBiochemistryProteolysisProcollagen N-EndopeptidaseProceedings of the National Academy of Sciences of the United States of America
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