Search results for " ACTIVATION"

showing 10 items of 1535 documents

Dietary polyunsaturated fatty acids reduce retinal stress induced by an elevation of intraocular pressure in rats.

2011

International audience; N-6 and n-3 polyunsaturated fatty acids (PUFAs) have been shown to prevent tissue release of inflammatory molecules. We have shown that a combination of n-6 and n-3 PUFAs is more efficient than single supplementations on the long-term consequences of intraocular pressure elevation. We hypothesized that such an association is also more effective during early retinal stress by modifying retinal proinflammatory prostaglandin and cytokine productions. Rats were supplemented for 3 months with n-6 PUFAs, n-3 PUFAs, or both n-6 and n-3 PUFAs. After 3 months, a surgical elevation of intraocular pressure was induced. Retinal morphometry and glial cell activation were evaluate…

MaleMESH : RNA MessengerMESH: Eicosapentaenoic AcidEndocrinology Diabetes and Metabolismmedicine.medical_treatment[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionInterleukin-1betaMESH: Dietary SupplementsMESH: Rats Sprague-DawleyRats Sprague-Dawleychemistry.chemical_compound0302 clinical medicineEndocrinologyMESH: Interleukin-1betaratMESH: AnimalsProstaglandin E2Prostaglandin E1MESH : Tumor Necrosis Factor-alphaMESH : Intraocular Pressure0303 health sciencesNutrition and DieteticsMESH : RatsMESH : NeurogliaMESH: RetinaMESH: Dinoprostonepression intraoculaireMESH: AlprostadilMESH: Docosahexaenoic AcidsBiochemistryEicosapentaenoic AcidDocosahexaenoic acidlipids (amino acids peptides and proteins)MESH: NeurogliaProstaglandin D2Cell activationNeurogliaMESH : Alprostadilmedicine.drugProstaglandin Emedicine.medical_specialtyMESH : DinoprostoneMESH : Interleukin-6Docosahexaenoic AcidsMESH: RatsMESH : MaleProstaglandinBiologyMESH : Interleukin-1betaDinoprostoneRetinaMESH : Diet03 medical and health sciencesMESH: DietMESH: Intraocular PressureInternal medicinemedicineMESH : Eicosapentaenoic AcidAnimalsMESH : Dietary SupplementsRNA MessengerAlprostadilprostanoids030304 developmental biologyMESH: RNA MessengerInterleukin-6Tumor Necrosis Factor-alphadietary polyunsatured fatty acidretinal stressMESH : RetinaRetinalN-6MESH: Interleukin-6MESH : Rats Sprague-Dawleyeye diseasesMESH: MaleMESH : Docosahexaenoic AcidsDietRatsN-3EndocrinologychemistryMESH: Tumor Necrosis Factor-alphaDietary Supplements030221 ophthalmology & optometryMESH : Animalssense organs[SDV.AEN]Life Sciences [q-bio]/Food and Nutritionintraocular pressure
researchProduct

The Genome of the Sea Urchin Strongylocentrotus purpuratus

2006

We report the sequence and analysis of the 814-megabase genome of the sea urchin Strongylocentrotus purpuratus , a model for developmental and systems biology. The sequencing strategy combined whole-genome shotgun and bacterial artificial chromosome (BAC) sequences. This use of BAC clones, aided by a pooling strategy, overcame difficulties associated with high heterozygosity of the genome. The genome encodes about 23,300 genes, including many previously thought to be vertebrate innovations or known only outside the deuterostomes. This echinoderm genome provides an evolutionary outgroup for the chordates and yields insights into the evolution of deuterostomes.

MaleMESH: Signal TransductionMESH: Sequence Analysis DNAMESH : Transcription FactorsMESH : Calcification PhysiologicGenomeMESH : Proteins0302 clinical medicineMESH : Embryonic DevelopmentMESH: Gene Expression Regulation DevelopmentalInnateMESH: Embryonic DevelopmentDevelopmentalNervous System Physiological PhenomenaMESH: AnimalsMESH: Proteins[SDV.BDD]Life Sciences [q-bio]/Development BiologyComplement ActivationComputingMilieux_MISCELLANEOUSMESH: Evolution MolecularMESH : Strongylocentrotus purpuratusGenetics0303 health sciencesMESH: Nervous System Physiological PhenomenaMultidisciplinaryGenomebiologyMedicine (all)MESH: Immunologic FactorsGene Expression Regulation DevelopmentalGenome projectMESH: Transcription FactorsMESH : Immunity InnateMESH : Complement ActivationMESH: GenesBacterial artificial chromosome (BAC)DeuterostomesStrongylocentrotus purpuratusVertebrate innovationsEchinodermMESH : Nervous System Physiological Phenomenaembryonic structuresMESH: Cell Adhesion MoleculesMESH : GenesMESH: Immunity InnateSequence AnalysisSignal TransductionMESH: Computational BiologyGenome evolutionMESH: Complement ActivationSequence analysisEvolutionMESH: Strongylocentrotus purpuratusMESH : MaleEmbryonic DevelopmentMESH : Immunologic FactorsArticleMESH: Calcification PhysiologicCalcificationMESH : Cell Adhesion MoleculesEvolution Molecular03 medical and health sciencesCalcification PhysiologicAnimalsImmunologic FactorsMESH: Genome[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyMESH : Evolution MolecularPhysiologicGeneStrongylocentrotus purpuratus[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular Biology030304 developmental biologyMESH : Signal TransductionBacterial artificial chromosomeImmunityMolecularComputational BiologyProteinsAnimals; Calcification Physiologic; Cell Adhesion Molecules; Complement Activation; Computational Biology; Embryonic Development; Evolution Molecular; Gene Expression Regulation Developmental; Genes; Immunity Innate; Immunologic Factors; Male; Nervous System Physiological Phenomena; Proteins; Signal Transduction; Strongylocentrotus purpuratus; Transcription Factors; Genome; Sequence Analysis DNA; Medicine (all); MultidisciplinaryDNASequence Analysis DNAbiology.organism_classificationStrongylocentrotus purpuratusImmunity InnateMESH: MaleGene Expression RegulationGenesMESH : AnimalsMESH : Gene Expression Regulation DevelopmentalMESH : GenomeCell Adhesion Molecules030217 neurology & neurosurgeryMESH : Computational BiologyTranscription FactorsMESH : Sequence Analysis DNA
researchProduct

Constitutive activation of JAK2 in mammary epithelium elevates Stat5 signalling, promotes alveologenesis and resistance to cell death, and contribute…

2011

Signalling through the janus kinase (JAK)/signal transducer and activator of transcription (Stat) pathway is required at different stages of mammary gland development, and this pathway is frequently hyper-activated in cancer, including tumours of the breast. Stats 3, 5 and 6 have important roles in the differentiation and survival of mammary alveolar cells, but somewhat paradoxically, both Stat3 and 5 can have oncogenic activity in the mammary gland. Constitutive activation of JAK2 could be anticipated to result in hyper-activation of Stats 1, 3, 5 and 6 with concomitant cell transformation, although the outcome is difficult to envisage, particularly since Stats 3 and 5 play opposing roles …

MaleMammary glandTransplantation HeterologousMutation MissenseMice NudeBreast NeoplasmsMammary Neoplasms AnimalMiceMammary Glands AnimalPregnancyhemic and lymphatic diseasesCell Line TumormedicineSTAT5 Transcription FactorAnimalsHumansLactationSTAT3Mammary Glands HumanMolecular BiologySTAT5Mice KnockoutOriginal PaperJanus kinase 2biologyCell DeathCell growthCell BiologyJanus Kinase 2Enzyme Activationmedicine.anatomical_structureCell Transformation Neoplasticbiology.proteinSTAT proteinCancer researchFemaleSignal transductionJanus kinaseNeoplasm TransplantationSignal Transduction
researchProduct

The Long-Term Effect of Sevoflurane on Neuronal Cell Damage and Expression of Apoptotic Factors After Cerebral Ischemia and Reperfusion in Rats

2006

We investigated the long-term effects of sevoflurane on histopathologic injury and key proteins of apoptosis in a rat hemispheric ischemia/reperfusion model. Sixty-four male Sprague-Dawley rats were randomly assigned to Group 1 (fentanyl and N2O/O2; control) and Group 2 (2.0 vol% sevoflurane and O2/air). Ischemia (45 min) was produced by unilateral common carotid artery occlusion plus hemorrhagic hypotension (mean arterial blood pressure 40 mm Hg). Animals were killed after 1, 3, 7, and 28 days. In hematoxylin and eosin-stained brain sections eosinophilic hippocampal neurons were counted. Activated caspase-3 and the apoptosis-regulating proteins Bax, Bcl-2, Mdm-2, and p53 were analyzed by i…

MaleMethyl Ethersmedicine.medical_specialtyH&E stainIschemiaCell CountHippocampal formationHippocampusNeuroprotectionSevofluraneBrain IschemiaRats Sprague-DawleySevofluraneInternal medicineEosinophilicmedicineAnimalsNeuronsCaspase 3business.industrymedicine.diseaseImmunohistochemistryRatsEnzyme ActivationNeuroprotective AgentsAnesthesiology and Pain MedicineBlood pressureEndocrinologyCaspasesCerebrovascular CirculationReperfusion InjuryAnesthesiaAnesthetics InhalationApoptosis Regulatory ProteinsbusinessBlood Flow VelocityImmunostainingmedicine.drugAnesthesia & Analgesia
researchProduct

Autoimmune skin inflammation is dependent on plasmacytoid dendritic cell activation by nucleic acids via TLR7 and TLR9

2010

Lupus-prone mice develop a chronic inflammatory response to cutaneous injury that depends on the production of type I interferon, TLR7, and TLR9.

MaleMice 129 StrainImmunologyGene ExpressionInflammationchemical and pharmacologic phenomenaMice Inbred StrainsReceptor Interferon alpha-betaBiologySkin DiseasesArticleProinflammatory cytokinePathogenesisTLR9MiceAutoimmune skin inflammationimmune system diseasesNucleic AcidsmedicineImmunology and AllergyAnimalsLupus Erythematosus SystemicReceptorskin and connective tissue diseasesTLR7SkinAutoimmune skin inflammation; TLR7; TLR9; plasmacytoid dendritic cells.Mice KnockoutPlasmacytoid dendritic cell activationLupus erythematosusReverse Transcriptase Polymerase Chain ReactionTLR9virus diseaseshemic and immune systemsTLR7DNADendritic Cellsmedicine.diseaseFlow CytometryMice Inbred C57BLplasmacytoid dendritic cells.Toll-Like Receptor 7Toll-Like Receptor 9ImmunologyMyeloid Differentiation Factor 88CytokinesFemalemedicine.symptomThe Journal of Experimental Medicine
researchProduct

Bilobalide, a constituent of Ginkgo biloba , inhibits NMDA-induced phospholipase A 2 activation and phospholipid breakdown in rat hippocampus

2000

In rat hippocampal slices superfused with magnesium-free buffer, glutamate (1 mM) caused the release of large amounts of choline due to phospholipid breakdown. This phenomenon was mimicked by N-methyl-D-aspartate (NMDA) in a calcium-sensitive manner and was blocked by NMDA receptor antagonists such as MK-801 and 7-chlorokynurenate. The NMDA-induced release of choline was not caused by activation of phospholipase D but was mediated by phospholipase A2 (PLA2) activation as the release of choline was accompanied by the formation of lyso-phosphatidylcholine (lyso-PC) and glycerophospho-choline (GPCh) and was blocked by 5-[2-(2-carboxyethyl)-4-dodecanoyl-3,5-dimethylpyrrol-1-yl]pentano ic acid, …

MaleMicrodialysisN-MethylaspartateMicrodialysisGlycineCyclopentanesPharmacologyHippocampal formationHippocampusReceptors N-Methyl-D-AspartatePhospholipases ACholinechemistry.chemical_compoundPhospholipase A2BilobalideSeizuresAnimalsCholineRats WistarFuransCells CulturedPhospholipidsPharmacologyPlants MedicinalDose-Response Relationship DrugbiologyPhospholipase DGlutamate receptorGinkgo bilobaLysophosphatidylcholinesGeneral MedicineGlycerylphosphorylcholineRatsEnzyme ActivationPhospholipases A2Ginkgolideschemistrybiology.proteinNMDA receptorDiterpenesNaunyn-Schmiedeberg's Archives of Pharmacology
researchProduct

Phenotypic and biochemical analysis of an international cohort of individuals with variants in NAA10 and NAA15.

2019

Abstract N-alpha-acetylation is one of the most common co-translational protein modifications in humans and is essential for normal cell function. NAA10 encodes for the enzyme NAA10, which is the catalytic subunit in the N-terminal acetyltransferase A (NatA) complex. The auxiliary and regulatory subunits of the NatA complex are NAA15 and Huntington-interacting protein (HYPK), respectively. Through a genotype-first approach with exome sequencing, we identified and phenotypically characterized 30 individuals from 30 unrelated families with 17 different de novo or inherited, dominantly acting missense variants in NAA10 or NAA15. Clinical features of affected individuals include variable levels…

MaleModels Molecular0301 basic medicineProtein ConformationMicrophthalmia0302 clinical medicineEnzyme StabilityMissense mutationN-Terminal Acetyltransferase EChildN-Terminal Acetyltransferase AExome sequencingGenetics (clinical)GeneticsbiologyGeneral MedicinePhenotypeRecombinant ProteinsChemistryPhenotypeChild PreschoolHMG-CoA reductaseCohortFemaleGeneral ArticleCorrigendumAdultNatA complexmedicine.medical_specialtyAdolescentGenotypeFrameshift mutationStructure-Activity RelationshipYoung Adult03 medical and health sciencesMolecular geneticsGeneticsmedicineHumansGenetic Predisposition to DiseaseGenetic TestingAlleleBiologyMolecular BiologyAllelesGenetic Association StudiesComputational BiologyFaciesGenetic VariationInfantmedicine.diseaseEnzyme ActivationLenz microphthalmia syndrome030104 developmental biologyGenetic LociMutationbiology.proteinHuman medicineBiomarkers030217 neurology & neurosurgeryNAA15Human molecular genetics
researchProduct

Distant Homology Modeling of LCAT and Its Validation through In Silico Targeting and In Vitro and In Vivo Assays

2013

LCAT (lecithin:cholesterol acyltransferase) catalyzes the transacylation of a fatty acid of lecithin to cholesterol, generating a cholesteryl ester and lysolecithin. The knowledge of LCAT atomic structure and the identification of the amino acids relevant in controlling its structure and function are expected to be very helpful to understand the enzyme catalytic mechanism, as involved in HDL cholesterol metabolism. However - after an early report in the late '90 s - no recent advance has been made about LCAT three-dimensional structure. In this paper, we propose an LCAT atomistic model, built following the most up-to-date molecular modeling approaches, and exploiting newly solved crystallog…

MaleModels MolecularProtein StructureDrug Research and DevelopmentProtein Conformationlcsh:MedicineBiologyBiochemistryCatalysisSubstrate SpecificityPhosphatidylcholine-Sterol O-AcyltransferaseMicechemistry.chemical_compoundEnzyme activatorTransacylationProtein structureDrug DiscoveryHydrolaseCatalytic triadBiochemical SimulationsMedicine and Health SciencesAnimalsHumansHomology modelingBiomacromolecule-Ligand Interactionslcsh:SciencePharmacologyBinding SitesPlasma ProteinsMultidisciplinarylcsh:RBiology and Life SciencesProteinsEnzyme structureEnzyme ActivationMolecular Docking SimulationchemistryBiochemistryMutationEnzyme StructureEnzymologyBiocatalysisCholesteryl esterlcsh:QResearch ArticleBiotechnologyPLoS ONE
researchProduct

Single cell detection of latent cytomegalovirus reactivation in host tissue

2011

The molecular mechanisms leading to reactivation of latent cytomegalovirus are not well understood. To study reactivation, the few cells in an organ tissue that give rise to reactivated virus need to be identified, ideally at the earliest possible time point in the process. To this end, mouse cytomegalovirus (MCMV) reporter mutants were designed to simultaneously express the red fluorescent protein mCherry and the secreted Gaussia luciferase (Gluc). Whereas Gluc can serve to assess infection at the level of individual mice by measuring luminescence in blood samples or by in vivo imaging, mCherry fluorescence offers the advatage of detection of infection at the single cell level. To visualiz…

MaleMuromegalovirusCytomegalovirusGene Expressionmedicine.disease_causeVirusHerpesviridaeGreen fluorescent proteinMiceGaussiaMuromegalovirusSingle-cell analysisGenes ReporterVirologyVirus latencymedicineAnimalsHumansLuciferasesLungMice Inbred BALB CbiologyHerpesviridae Infectionsbiology.organism_classificationmedicine.diseaseVirologyVirus LatencyDisease Models AnimalLuminescent ProteinsCytomegalovirus InfectionsHost-Pathogen InteractionsFemaleVirus ActivationSingle-Cell AnalysismCherryJournal of General Virology
researchProduct

Liver Sinusoidal Endothelial Cells Are a Site of Murine Cytomegalovirus Latency and Reactivation▿

2009

ABSTRACT Latent cytomegalovirus (CMV) is frequently transmitted by organ transplantation, and its reactivation under conditions of immunosuppressive prophylaxis against graft rejection by host-versus-graft disease bears a risk of graft failure due to viral pathogenesis. CMV is the most common cause of infection following liver transplantation. Although hematopoietic cells of the myeloid lineage are a recognized source of latent CMV, the cellular sites of latency in the liver are not comprehensively typed. Here we have used the BALB/c mouse model of murine CMV infection to identify latently infected hepatic cell types. We performed sex-mismatched bone marrow transplantation with male donors …

MaleMuromegalovirusMyeloidGenes ViralViral pathogenesisImmunologymedicine.disease_causeMicrobiologyHerpesviridaeVirusMiceAntigenBetaherpesvirinaeVirologyVirus latencymedicineAnimalsMice Inbred BALB CbiologyGene Expression ProfilingEndothelial Cellsbiology.organism_classificationmedicine.diseaseVirologyVirus LatencyHaematopoiesismedicine.anatomical_structureLiverInsect ScienceImmunologyPathogenesis and ImmunityFemaleVirus Activation
researchProduct