Search results for "Reporter"

showing 6 items of 166 documents

Interleukin 10 restores lipopolysaccharide-induced alterations in synaptic plasticity probed by repetitive magnetic stimulation

2020

Systemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess and quantify inflammation-associated alterations in synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic inflammation alters the ability of hippocampal neurons to express synaptic plasticity, i.e., the long-term potentiation (LTP) of excitatory neurotransmission. Here, we tested whether synaptic plasticity induced by repetitive magnetic stimulation (rMS), a non-invasive brain stimulation technique used in clinical practice, is affected by LPS-induc…

lcsh:Immunologic diseases. AllergyLipopolysaccharides0301 basic medicinenon-invasive brain stimulationInterleukin-1betaImmunologyTNFα-reporter mouseMice TransgenicStimulationNeurotransmissionHippocampusSynaptic TransmissionneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineGenes Reportertranscranial magnetic stimulationAnimalsImmunology and Allergyddc:610NeuroinflammationOriginal ResearchInflammationNeuronsNeuronal Plasticitysynaptic plasticityInterleukin-6Tumor Necrosis Factor-alphaChemistryLong-term potentiationInterleukin-10Mice Inbred C57BLOrganoids030104 developmental biologyBrain stimulationSynaptic plasticityExcitatory postsynaptic potentialTumor necrosis factor alphaMicrogliainterleukin 10lcsh:RC581-607Neuroscience030217 neurology & neurosurgery
researchProduct

Induction of the adrenoleukodystrophy-related gene (ABCD2) by thyromimetics.

2009

X-linked adrenoleukodystrophy (X-ALD) is a peroxisomal disorder caused by mutations in the ABCD1 (ALD) gene. The ABCD2 gene, its closest homolog, has been shown to compensate for ABCD1 deficiency when overexpressed. We previously demonstrated that the ABCD2 promoter contains a functional thyroid hormone response element. Thyroid hormone (T3) through its receptor TRbeta can induce hepatic Abcd2 expression in rodents and transiently normalize the VLCFA level in fibroblasts of Abcd1 null mice. In a therapeutic perspective, the use of selective agonists of TRbeta should present the advantage to be devoid of side effects, at least concerning the cardiotoxicity associated to TRalpha activation. I…

medicine.medical_specialtyThyroid HormonesEndocrinology Diabetes and MetabolismClinical BiochemistryBiologyAcetatesATP Binding Cassette Transporter Subfamily DTransfectionBiochemistryEndocrinologyDownregulation and upregulationPhenolsInternal medicinePeroxisomal disorderGene expressionChlorocebus aethiopsmedicineAnimalsHumansReceptorAdrenoleukodystrophyMolecular BiologyHormone response elementReporter geneGlyoxylatesCell BiologyTransfectionmedicine.diseaseCell biologyRatsUp-RegulationEndocrinologyCOS CellsMolecular MedicineTriiodothyronineAdrenoleukodystrophyATP-Binding Cassette TransportersThe Journal of steroid biochemistry and molecular biology
researchProduct

A common mechanism of action of the selective serotonin reuptake inhibitors citalopram and fluoxetine: Reversal of chronic psychosocial stress-induce…

2010

The transcription factor CREB regulates adaptive responses like memory consolidation, addiction, and synaptic refinement. Recently, chronic psychosocial stress as animal model of depression has been shown to stimulate CREB transcriptional activity in the brain; this stimulation was prevented by treatment with the antidepressant imipramine, which inhibits both noradrenaline and serotonin reuptake. However, it was unknown whether the selective inhibition of serotonin reuptake is sufficient for inhibition of stress-induced CREB activation, as it is for the clinical antidepressant effect. Therefore, the effect of two selective serotonin reuptake inhibitors (SSRIs), citalopram and fluoxetine, wa…

medicine.medical_specialtyTranscription GeneticMice TransgenicCitalopramBiologyCitalopramCREBImipramineDrug Administration ScheduleMice03 medical and health sciences0302 clinical medicineGenes ReporterCREB in cognitionFluoxetineInternal medicinemedicineAnimalsPhosphorylationCyclic AMP Response Element-Binding ProteinTranscription factor030304 developmental biologyPharmacology0303 health sciencesFluoxetineBrain3. Good healthEndocrinologyGene Expression RegulationMechanism of actionbiology.proteinAntidepressantmedicine.symptomSelective Serotonin Reuptake InhibitorsStress Psychological030217 neurology & neurosurgerymedicine.drugEuropean Journal of Pharmacology
researchProduct

Murine bone marrow-derived mast cells as potent producers of IL-9: costimulatory function of IL-10 and kit ligand in the presence of IL-1.

2000

Abstract Recently, the Th2-type cytokine IL-9 was identified by genetic mapping analyses as a key mediator that determines the susceptibility to asthma. This has been further supported by data from IL-9-transgenic mice in which the overexpression of IL-9 in the lung causes airway inflammation, mast cell hyperplasia, and bronchial hyperresponsiveness. In an accompanying paper, we demonstrate that murine bone marrow-derived mast cells (BMMC) after stimulation with either ionomycin, a combination of ionomycin and IL-1, or via IgE-Ag complexes and IL-1 are very potent producers of IL-9. Herein we show that a dramatic increase of IL-9 production is observed when BMMC activated with ionomycin/IL-…

medicine.medical_treatmentImmunologyEndogenyStem cell factorBone Marrow CellsBiologychemistry.chemical_compoundMiceAdjuvants ImmunologicmedicineImmunology and AllergyAnimalsMast CellsRNA MessengerReporter geneMice Inbred BALB CStem Cell FactorInterleukin-9TransfectionMolecular biologyInterleukin-10Interleukin 10medicine.anatomical_structureCytokinechemistryGene Expression RegulationIonomycinImmunologyBone marrow5' Untranslated RegionsInterleukin-1Journal of immunology (Baltimore, Md. : 1950)
researchProduct

Genomic structure and promoter analysis of pathogen-inducedrepatgenes fromSpodoptera exigua

2009

The repat gene family encodes midgut proteins overexpressed in response to pathogen infection in the lepidopteran Spodoptera exigua. Up-regulation of repat genes has been observed after challenging the larvae with both Bacillus thuringiensis toxins and after infection with the baculovirus Autographa californica multiple nucleopolyhedrovirus. In our study, PCR amplification of the genomic region and genome walking were used to obtain the genomic structure and the sequence of the 5'-upstream region of repat1 and repat2, two of the most phylogenetically distant members of the repat family. A similar gene structure between repat1 and repat2 has been found, with conserved exon-intron positions a…

virusesGenome InsectMolecular Sequence DataGenes InsectSpodopteraBiologySpodopteraOpen Reading FramesGenes ReporterIntron-mediated enhancementGene expressionGeneticsPrimer walkingAnimalsGene familyCloning MolecularPromoter Regions GeneticMolecular BiologyGeneGeneticsBase SequencefungiIntronPromoterbiology.organism_classificationMolecular biologyInsect ScienceSequence AlignmentInsect Molecular Biology
researchProduct

Enhancement of hepatitis C virus RNA replication by cell culture-adaptive mutations.

2001

ABSTRACT Studies of the Hepatitis C virus (HCV) replication cycle have been made possible with the development of subgenomic selectable RNAs that replicate autonomously in cultured cells. In these replicons the region encoding the HCV structural proteins was replaced by the neomycin phosphotransferase gene, allowing the selection of transfected cells that support high-level replication of these RNAs. Subsequent analyses revealed that, within selected cells, HCV RNAs had acquired adaptive mutations that increased the efficiency of colony formation by an unknown mechanism. Using a panel of replicons that differed in their degrees of cell culture adaptation, in this study we show that adaptive…

virusesImmunologyCell Culture TechniquesRNA-dependent RNA polymeraseReplicationHepacivirusBiologyViral Nonstructural ProteinsOrigin of replicationVirus ReplicationMicrobiologyReplication factor CControl of chromosome duplicationGenes ReporterVirologyTumor Cells CulturedHumansRepliconLuciferasesGeneRNAVirologyAdaptation PhysiologicalViral replicationInsect ScienceMutationRNA ViralRepliconJournal of virology
researchProduct