Search results for "Knockout"

showing 10 items of 806 documents

The Tick Salivary Protein Sialostatin L Inhibits the Th9-Derived Production of the Asthma-Promoting Cytokine IL-9 and Is Effective in the Prevention …

2012

Abstract Ticks developed a multitude of different immune evasion strategies to obtain a blood meal. Sialostatin L is an immunosuppressive cysteine protease inhibitor present in the saliva of the hard tick Ixodes scapularis. In this study, we demonstrate that sialostatin L strongly inhibits the production of IL-9 by Th9 cells. Because we could show recently that Th9-derived IL-9 is essentially involved in the induction of asthma symptoms, sialostatin L was used for the treatment of experimental asthma. Application of sialostatin L in a model of experimental asthma almost completely abrogated airway hyperresponsiveness and eosinophilia. Our data suggest that sialostatin L can prevent experime…

MaleSalivaIxodidaemedicine.medical_treatmentImmunologyEnzyme-Linked Immunosorbent AssayCell SeparationBiologyReal-Time Polymerase Chain ReactionArticleNeutralizationMiceImmune systemT-Lymphocyte SubsetsmedicineAnimalsImmunology and AllergyEosinophiliaAsthmaMice KnockoutMice Inbred BALB CReverse Transcriptase Polymerase Chain ReactionInterleukin-9Flow Cytometrymedicine.diseaseCystatinsCysteine proteaseAsthmarespiratory tract diseasesDisease Models AnimalCytokineIxodes scapularisImmunologyCytokinesFemalemedicine.symptom
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TLR4 response mediates ethanol-induced neurodevelopment alterations in a model of fetal alcohol spectrum disorders

2017

Background Inflammation during brain development participates in the pathogenesis of early brain injury and cognitive dysfunctions. Prenatal ethanol exposure affects the developing brain and causes neural impairment, cognitive and behavioral effects, collectively known as fetal alcohol spectrum disorders (FASD). Our previous studies demonstrate that ethanol activates the innate immune response and TLR4 receptor and causes neuroinflammation, brain damage, and cognitive defects in the developmental brain stage of adolescents. We hypothesize that by activating the TLR4 response, maternal alcohol consumption during pregnancy triggers the release of cytokines and chemokines in both the maternal …

MaleSerum0301 basic medicineChemokineDevelopmental Disabilitiesmedicine.medical_treatmentlcsh:RC346-429MiceMyelin0302 clinical medicineNeuroinflammationPregnancyTLR4Maternal BehaviorFetal alcohol spectrum disordersMice KnockoutMicrogliabiologyGeneral NeuroscienceAge FactorsBrainCerebral cortexBehavior impairmentsmedicine.anatomical_structureCytokineNeurologyPrenatal Exposure Delayed EffectsCytokinesFemalemedicine.symptomMyelin ProteinsAmniotic fluidmedicine.medical_specialtyOffspringImmunologyNerve Tissue ProteinsBrain damage03 medical and health sciencesCellular and Molecular NeuroscienceInternal medicineAvoidance LearningmedicineAnimalsMaze Learninglcsh:Neurology. Diseases of the nervous systemNeuroinflammationEthanolbusiness.industryResearchBody WeightCentral Nervous System DepressantsMice Inbred C57BLToll-Like Receptor 4Disease Models AnimalMicroscopy Electron030104 developmental biologyEndocrinologyAnimals NewbornPrenatal ethanol exposureImmunologybiology.proteinTLR4business030217 neurology & neurosurgeryJournal of Neuroinflammation
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Monocytes derived from humanized neonatal NOD/SCID/IL2Rγ(null) mice are phenotypically immature and exhibit functional impairments.

2012

Trials of immune-modulating drugs in septic patients have mostly failed to demonstrate clinical efficacy. Thus, we sought to generate a surrogate model of myelomonocytic lineage differentiation that would potentially allow sepsis induction and preclinical testing of anti-inflammatory drugs. Comparing transplantation of cord blood-derived stem cells in neonatal NOD/SCID/IL2Rγ(null) (neonatal huNSG) mice with transplantation of adult peripheral mobilized stem cells into adult NSG (adult huNSG) recipients, we demonstrate that myelomonocytic lineage differentiation in neonatal huNSG mice is retarded and monocytes are phenotypically immature with respect to HLA-DR expression and the emergence of…

MaleT-LymphocytesImmunologyPopulationLipopolysaccharide ReceptorsNodMice SCIDBiologyLymphocyte ActivationMonocytesImmunophenotypingMicePhagocytosisMice Inbred NODmedicineImmunology and AllergyAnimalsHumansCell LineageeducationCD86Mice Knockouteducation.field_of_studyMonocyteCell DifferentiationGeneral MedicineTransplantationmedicine.anatomical_structurePhenotypeImmunologyCytokinesCytokine secretionFemaleStem cellInflammation MediatorsCD80Interleukin Receptor Common gamma SubunitHuman immunology
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Obesity causes PGC‐1α deficiency in the pancreas leading to marked IL‐6 upregulation via NF‐κB in acute pancreatitis

2019

Obesity is associated with local and systemic complications in acute pancreatitis. PPARγ coactivator 1α (PGC-1α) is a transcriptional coactivator and master regulator of mitochondrial biogenesis that exhibits dysregulation in obese subjects. Our aims were: (1) to study PGC-1α levels in pancreas from lean or obese rats and mice with acute pancreatitis; and (2) to determine the role of PGC-1α in the inflammatory response during acute pancreatitis elucidating the signaling pathways regulated by PGC-1α. Lean and obese Zucker rats and lean and obese C57BL6 mice were used first; subsequently, wild-type and PGC-1α knockout (KO) mice with cerulein-induced pancreatitis were used to assess the inflam…

MaleTaurocholic Acid0301 basic medicinemedicine.medical_specialtyPGC-1αPathology and Forensic Medicine03 medical and health sciencesDownregulation and upregulationInternal medicineAnimalsMedicineObesityPhosphorylationInterleukin 6PancreasCeruletideMice KnockoutIL-6biologyp65Interleukin-6business.industryNF-kappa BTranscription Factor RelAmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRats ZuckerUp-Regulation3. Good healthMice Inbred C57BLDisease Models Animal030104 developmental biologyEndocrinologymedicine.anatomical_structureMitochondrial biogenesisPancreatitisbiology.proteinPancreatitisAcute pancreatitisPPARGC1AbusinessPancreasCeruletideSignal TransductionThe Journal of Pathology
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Thyroid hormone induction of the adrenoleukodystrophy-related gene (ABCD2).

2003

X-linked adrenoleukodystrophy (X-ALD) is a demyelinating disorder associated with impaired very-long-chain fatty-acid (VLCFA) beta-oxidation caused by mutations in the ABCD1 (ALD) gene that encodes a peroxisomal membrane ABC transporter. ABCD2 (ALDR) displays partial functional redundancy because when overexpressed, it is able to correct the X-ALD biochemical phenotype. The ABCD2 promoter contains a putative thyroid hormone-response element conserved in rodents and humans. In this report, we demonstrate that the element is capable of binding retinoid X receptor and 3,5,3'-tri-iodothyronine (T3) receptor (TRbeta) as a heterodimer and mediating T3 responsiveness of ABCD2 in its promoter conte…

MaleThyroid HormonesReceptors Retinoic AcidGene ExpressionATP-binding cassette transporterRetinoid X receptorRats Sprague-DawleyMiceABCD3Gene expressionABCD2medicineAnimalsHumansReceptorAdrenoleukodystrophyPromoter Regions GeneticGeneCells CulturedRepetitive Sequences Nucleic AcidPharmacologyChemokine CCL22Mice KnockoutReceptors Thyroid Hormonebiologymedicine.diseaseCell biologyRatsUp-RegulationOligodendrogliaRetinoid X ReceptorsLiverAstrocytesChemokines CCbiology.proteinCancer researchMolecular MedicineTriiodothyronineAdrenoleukodystrophyChemokine CCL17Transcription FactorsMolecular pharmacology
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Short-term adaptation of conditioned fear responses through endocannabinoid signaling in the central amygdala

2010

International audience; Both, the cannabinoid receptor type 1 (CB1) and the central nucleus of the amygdala (CeA) are known to play crucial roles in the processing of fear and anxiety, whereby they appear to be especially involved in the control of fear states. However, in contrast to many other brain regions including the cortical subregions of the amygdala, the existence of CB1 in the CeA remains enigmatic. Here we show that CB1 is expressed in the CeA of mice and that CB1 in the CeA mediates short-term synaptic plasticity, namely depolarization-induced suppression of excitation (DSE) and inhibition (DSI). Moreover, the CB1 antagonist AM251 increased both excitatory and inhibitory postsyn…

MaleTime FactorsAction PotentialsAnxietyExtinction PsychologicalGABA AntagonistsPropanolaminesMice0302 clinical medicinePiperidinesReceptor Cannabinoid CB1Adaptation PsychologicalConditioning PsychologicalMoodFear conditioningHabituationStress DisordersMice Knockout0303 health sciencesBehavior AnimalCentral nucleus of the amygdalaValineFearExtinctionAmygdalaPyridazinesPsychiatry and Mental healthmedicine.anatomical_structureOriginal ArticlePsychologypsychological phenomena and processesSignal TransductionSensory Receptor CellsNeurophysiologyIn Vitro TechniquesInhibitory postsynaptic potentialAmygdala03 medical and health sciencesQuinoxalinesCannabinoid Receptor ModulatorsmedicineAnimalsMaze Learning030304 developmental biologyPharmacologyFear processing in the brainLearning & MemoryCannabinoidsExtinction (psychology)Phosphinic AcidsElectric StimulationMice Inbred C57BLGene Expression Regulationnervous systemSynaptic plasticityPyrazolesNeuroscienceExcitatory Amino Acid Antagonists030217 neurology & neurosurgeryEndocannabinoidsConditioning
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Plasma membrane Ca2+ ATPase 4 is required for sperm motility and male fertility.

2004

Calcium and Ca(2+)-dependent signals play a crucial role in sperm motility and mammalian fertilization, but the molecules and mechanisms underlying these Ca(2+)-dependent pathways are incompletely understood. Here we show that homozygous male mice with a targeted gene deletion of isoform 4 of the plasma membrane calcium/calmodulin-dependent calcium ATPase (PMCA), which is highly enriched in the sperm tail, are infertile due to severely impaired sperm motility. Furthermore, the PMCA inhibitor 5-(and-6)-carboxyeosin diacetate succinimidyl ester reduced sperm motility in wild-type animals, thus mimicking the effects of PMCA4 deficiency on sperm motility and supporting the hypothesis of a pivot…

MaleTime FactorsBiochemistryMiceTestisProtein IsoformsCloning MolecularCation Transport Proteinsreproductive and urinary physiologySperm motilityMice KnockoutRecombination GeneticReverse Transcriptase Polymerase Chain ReactionPlasma Membrane Calcium-Transporting ATPasesFluoresceinsTransport proteinCell biologyBlotting SouthernBiochemistrySperm Motilityendocrine systemDNA ComplementaryGenotypeBlotting WesternMolecular Sequence Datachemistry.chemical_elementSuccinimidesCalcium-Transporting ATPasesFertilization in VitroCalciumBiologyPlasma Membrane Calcium-Transporting ATPasesAnimalsHumansMolecular BiologyFluorescent DyesCalcium metabolismModels Geneticurogenital systemCell BiologyBlotting NorthernSpermProtein Structure TertiaryRatsCalcium ATPaseAlternative SplicingFertilitychemistryMicroscopy FluorescencePlasma membrane Ca2+ ATPaseCalciumThe Journal of biological chemistry
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Fibrate induction of the adrenoleukodystrophy-related gene (ABCD2)

2001

X-linked adrenoleukodystrophy (X-ALD) is a neurodegenerative disease due to a defect in the ABCD1 (ALD) gene. ABCD1, and the two close homologues ABCD2 (ALDR) and ABCD3 (PMP70), are genes encoding ATP-binding cassette half-transporters of the peroxisomal membrane. As overexpression of the ABCD2 or ABCD3 gene can reverse the biochemical phenotype of X-ALD (reduced beta-oxidation of very-long-chain fatty acids), pharmacological induction of these partially redundant genes may represent a therapeutic approach to X-ALD. We previously reported that the ABCD2 and ABCD3 genes could be strongly induced by fibrates, which are hypolipidaemic drugs and peroxisome-proliferators in rodents. We provide e…

MaleTranscription GeneticMolecular Sequence DataResponse elementReceptors Cytoplasmic and NuclearATP-binding cassette transporterATP Binding Cassette Transporter Subfamily DBiochemistryMiceFenofibrateABCD3Sequence Homology Nucleic AcidABCD2medicineAnimalsHumansRats WistarAdrenoleukodystrophyPromoter Regions GeneticGeneHypolipidemic AgentsMice KnockoutBase SequencebiologyDNATransfectionPeroxisomemedicine.diseaseMolecular biologyRatsGene Expression Regulationbiology.proteinATP-Binding Cassette TransportersAdrenoleukodystrophyTranscription FactorsEuropean Journal of Biochemistry
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Mandibular-pelvic-patellar syndrome (mpp) is a novel pitx1-related disorder due to alteration of pitx1 transactivation ability

2020

International audience; PITX1 is a homeobox transcription factor essential for hindlimb morphogenesis. Two PITX1-related human disorders have been reported to date: PITX1 ectopic expression causes Liebenberg syndrome, characterized by malformation of upper limbs showing a "lower limb" appearance; PITX1 deletions or missense variation cause a syndromic picture including clubfoot, tibial hemimelia, and preaxial polydactyly. We report two novel PITX1 missense variants, altering PITX1 transactivation ability, in three individuals from two unrelated families showing a distinct recognizable autosomal dominant syndrome, including first branchial arch, pelvic, patellar, and male genital abnormaliti…

MaleTranscriptional ActivationPathologymedicine.medical_specialtyHindlimb morphogenesis[SDV]Life Sciences [q-bio]Mutation MissensepelvisBiologyPierre-Robin03 medical and health sciencesTransactivationGeneticsmedicineMissense mutationAnimalsHumansPaired Box Transcription FactorsChildPITX1Genetics (clinical)030304 developmental biologyMice Knockoutcleft palate0303 health sciencesBone Diseases Developmental030305 genetics & heredityPreaxial polydactylyInfant NewbornLiebenberg syndromemedicine.disease3. Good healthgenitalpatella[SDV.GEN.GH]Life Sciences [q-bio]/Genetics/Human geneticsChild PreschoolHomeoboxEctopic expressionHaploinsufficiency
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Creating a conditional mutation of Wnt-1 by antisense transgenesis provides evidence that Wnt-1 is not essential for spermatogenesis.

1993

We have used mice transgenic for an antisense construct for Wnt-1 to study the role of this gene in post-meiotic sperm development. The human PGK-2 promoter provided levels of Wnt-1 antisense mRNA in testes in 5 transgenic lines greatly in excess of Wnt-1 mRNA concentrations, and Wnt-1 mRNA levels were greatly decreased in the lines, by 98% in three of them. There was a general correlation between copy number of the insert, levels of antisense RNA, and decreases in mRNA. There was little effect of the antisense transgene on fertility or testicular histology suggesting that normal levels of Wnt-1 transcript are not essential for spermatogenesis.

MaleTransgeneRecombinant Fusion ProteinsMolecular Sequence DataMice Inbred StrainsMice TransgenicWnt1 ProteinBiologyMiceProto-Oncogene ProteinsGene expressionTestisGeneticsAnimalsRNA AntisenseRNA MessengerPromoter Regions GeneticSpermatogenesisRegulation of gene expressionMice KnockoutMessenger RNABase SequenceWnt signaling pathwayRNACell BiologyZebrafish ProteinsMolecular biologyAntisense RNATransgenesisMice Inbred C57BLWnt ProteinsPhosphoglycerate KinaseFertilityGene Expression RegulationOrgan SpecificityDevelopmental BiologyDevelopmental genetics
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