Search results for "blotting"

showing 10 items of 899 documents

Permeability properties of a three-cell type in vitro model of blood-brain barrier.

2005

We previously found that RBE4.B brain capillary endothelial cells (BCECs) form a layer with blood‐brain barrier (BBB) properties if co‐cultured with neurons for at least one week. As astrocytes are known to modulate BBB functions, we further set a culture system that included RBE4.B BCECs, neurons and astrocytes. In order to test formation of BBB, we measured the amount of (3)H‐sucrose able to cross the BCEC layer in this three‐cell type model of BBB. Herein we report that both neurons and astrocytes induce a decrease in the permeability of the BCEC layer to sucrose. These effects are synergic as if BCECs are cultured with both neurons and astrocytes for 5 days, permeability to sucrose decr…

SucroseCell typeTime FactorsBlotting WesternVascular permeabilityBiologyBlood–brain barrierOccludinArticleCapillary PermeabilityOccludinmedicineAnimalsRats WistarCell Line TransformedNeuronsBrainEndothelial CellsMembrane ProteinsCell BiologyPermeationblood-brain barrier cortical neurons astrocytes brain capillary endothelial cells RBE4.B occludin.Coculture TechniquesRatsmedicine.anatomical_structurenervous systemMembrane proteinBiochemistryBlood-Brain BarrierPermeability (electromagnetism)Astrocytescardiovascular systembiology.proteinBiophysicsMolecular MedicineAntibody
researchProduct

Echovirus 1 Endocytosis into Caveosomes Requires Lipid Rafts, Dynamin II, and Signaling EventsV⃞

2004

Binding of echovirus 1 (EV1, a nonenveloped RNA virus) to the α2β1 integrin on the cell surface is followed by endocytic internalization of the virus together with the receptor. Here, video-enhanced live microscopy revealed the rapid uptake of fluorescently labeled EV1 into mobile, intracellular structures, positive for green fluorescent protein-tagged caveolin-1. Partial colocalization of EV1 with SV40 (SV40) and cholera toxin, known to traffic via caveosomes, demonstrated that the vesicles were caveosomes. The initiation of EV1 infection was dependent on dynamin II, cholesterol, and protein phosphorylation events. Brefeldin A, a drug that prevents SV40 transport, blocked the EV1 infection…

SucroseTime FactorsvirusesEndocytic cycleDynamin IIchemistry.chemical_compoundDynamin IIPhosphorylationInternalizationCytoskeletonIn Situ HybridizationIn Situ Hybridization Fluorescencemedia_commonGenes Dominant0303 health sciencesMicroscopy Videobiology030302 biochemistry & molecular biologyArticlesBrefeldin AEndocytosisCell biologyEnterovirus B HumanCholesterolRNA ViralElectrophoresis Polyacrylamide GelProtein BindingSignal TransductionCholera Toxinmedia_common.quotation_subjectIntegrinGreen Fluorescent ProteinsImmunoblottingEndocytosisTransfectionCell Line03 medical and health sciencesCapsidMembrane MicrodomainsViral entryCentrifugation Density GradientAnimalsMolecular Biology030304 developmental biologyBinding SitesBrefeldin ACell MembraneCell BiologyKineticschemistryViral replicationMicroscopy Fluorescencebiology.protein
researchProduct

Topotecan triggers apoptosis in p53-deficient cells by forcing degradation of XIAP and survivin thereby activating caspase-3-mediated Bid cleavage.

2009

The topoisomerase I inhibitor topotecan (TPT) is used in the therapy of different tumors including high-grade gliomas. We previously showed that TPT-induced apoptosis depends on p53 with p53 wild-type (wt) cells being more resistant because of p53-controlled degradation of topoisomerase I. Here, we show that p53-deficient (p53(-/-)) fibroblasts undergo excessive mitochondrial apoptosis featuring H2AX phosphorylation, Bcl-x(L) decline, cytochrome c release, caspase-9/-3/-2 activation, and cleavage of Bid. In wt and apaf-1(-/-) cells, caspase-2 did not become activated and Bid was not cleaved. In addition, p53(-/-) cells cotreated with TPT and caspase-3 inhibitor showed neither caspase-2 acti…

SurvivinBlotting WesternDown-RegulationCaspase 3ApoptosisX-Linked Inhibitor of Apoptosis ProteinBiologyTopoisomerase-I InhibitorInhibitor of apoptosisTransfectionInhibitor of Apoptosis ProteinsHistonesMiceCell Line TumorSurvivinAnimalsHumansPhosphorylationRNA Small InterferingPharmacologyMice KnockoutCaspase 3Caspase 2TransfectionFibroblastsFlow CytometryMolecular biologyXIAPMice Inbred C57BLRepressor ProteinsApoptotic Protease-Activating Factor 1ApoptosisCancer researchMolecular MedicineApoptosomeTopoisomerase I InhibitorsTumor Suppressor Protein p53TopotecanMicrotubule-Associated ProteinsBH3 Interacting Domain Death Agonist ProteinThe Journal of pharmacology and experimental therapeutics
researchProduct

CB(1) signaling in forebrain and sympathetic neurons is a key determinant of endocannabinoid actions on energy balance

2010

The endocannabinoid system (ECS) plays a critical role in obesity development. The pharmacological blockade of cannabinoid receptor type 1 (CB(1)) has been shown to reduce body weight and to alleviate obesity-related metabolic disorders. An unsolved question is at which anatomical level CB(1) modulates energy balance and the mechanisms involved in its action. Here, we demonstrate that CB(1) receptors expressed in forebrain and sympathetic neurons play a key role in the pathophysiological development of diet-induced obesity. Conditional mutant mice lacking CB(1) expression in neurons known to control energy balance, but not in nonneuronal peripheral organs, displayed a lean phenotype and res…

Sympathetic Nervous SystemPhysiologymedicine.medical_treatmentHUMDISEASEFluorescent Antibody TechniqueBody TemperatureMice0302 clinical medicineReceptor Cannabinoid CB1Cannabinoid receptor type 1ReceptorIn Situ HybridizationMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionCB(1)ThermogenesisEndocannabinoid systemOBESITYCB1 knock outlipids (amino acids peptides and proteins)CB(1); CANNABINOID RECEPTOR; OBESITY; ENDOCANNABINOID SYSTEM; METABOLIC DISORDERSSignal Transductionmedicine.medical_specialtyforebrainImmunoblottingCitrate (si)-SynthaseIn situ hybridizationHyperphagiaBiologyDNA MitochondrialModels BiologicalENDOCANNABINOID SYSTEMMOLNEURONO03 medical and health sciencesProsencephalonLipid oxidationInternal medicineMETABOLIC DISORDERSmedicineAnimalsMolecular BiologyCANNABINOID RECEPTOR030304 developmental biologyAnalysis of VarianceX-Ray MicrotomographyCell Biologyendocannabinoidenergy balanceEndocrinologynervous systemsympathetic neuronsForebrainCannabinoidEnergy Metabolismendocannabinoid; forebrain; sympathetic neurons; energy balance; CB1 knock outNeuroscienceThermogenesis030217 neurology & neurosurgery
researchProduct

Neuronal nitric oxide synthase modulates maturation of human dendritic cells.

2010

AbstractDendritic cells (DCs) are the most potent APCs of the immune system. Understanding the intercellular and intracellular signaling processes that lead to DC maturation is critical for determining how these cells initiate T cell-mediated immune processes. NO synthesized by the inducible NO synthase (iNOS) is important for the function of murine DCs. In our study, we investigated the regulation of the arginine/NO-system in human monocyte-derived DCs. Maturation of DCs induced by inflammatory cytokines (IL-1β, TNF, IL-6, and PGE2) resulted in a pronounced expression of neuronal NOS (nNOS) but only minimal levels of iNOS and endothelial NOS were detected in human mature DCs. In addition, …

T cellCellular differentiationImmunologyImmunoblottingchemical and pharmacologic phenomenaEnzyme-Linked Immunosorbent AssayCell SeparationNitric Oxide Synthase Type IBiologyEndothelial NOSLymphocyte ActivationNitric OxideProinflammatory cytokineCell LineImmune systemmedicineImmunology and AllergyHumansAutocrine signallingMHC class IIReverse Transcriptase Polymerase Chain ReactionCell DifferentiationDendritic CellsFlow CytometryCell biologymedicine.anatomical_structureCell culturebiology.proteinCytokinesJournal of immunology (Baltimore, Md. : 1950)
researchProduct

Cannabinoid CB1 receptor in dorsal telencephalic glutamatergic neurons: distinctive sufficiency for hippocampus-dependent and amygdala-dependent syna…

2013

A major goal in current neuroscience is to understand the causal links connecting protein functions, neural activity, and behavior. The cannabinoid CB1 receptor is expressed in different neuronal subpopulations, and is engaged in fine-tuning excitatory and inhibitory neurotransmission. Studies using conditional knock-out mice revealed necessary roles of CB1 receptor expressed in dorsal telencephalic glutamatergic neurons in synaptic plasticity and behavior, but whether this expression is also sufficient for brain functions is still to be determined. We applied a genetic strategy to reconstitute full wild-type CB1 receptor functions exclusively in dorsal telencephalic glutamatergic neurons a…

TelencephalonCannabinoid receptorLightBlotting WesternHippocampusGlutamic AcidBiologyNeurotransmissionAnxietyReal-Time Polymerase Chain ReactionAmygdalaHippocampus03 medical and health sciencesGlutamatergicMice0302 clinical medicineReceptor Cannabinoid CB1medicineExcitatory Amino Acid AgonistsAnimalsFear conditioning030304 developmental biologyMice KnockoutNeurons0303 health sciencesKainic AcidNeuronal PlasticityBehavior AnimalGeneral NeuroscienceArticlesAmygdalaEndocannabinoid systemImmunohistochemistryElectrophysiological PhenomenaMice Inbred C57BLmedicine.anatomical_structurenervous systemSynaptic plasticitySynapsesRNAlipids (amino acids peptides and proteins)Neuroscience030217 neurology & neurosurgerypsychological phenomena and processesJournal of Neuroscience
researchProduct

Glutathione regulates telomerase activity in 3T3 fibroblasts.

2004

Changes in telomerase activity have been associated either with cancer, when activity is increased, or with cell cycle arrest when it is decreased. We report that glutathione, a physiological antioxidant present at high intracellular concentrations, regulates telomerase activity in cells in culture. Telomerase activity increases in 3T3 fibroblasts before exponential cell growth. The peak of telomerase activity takes place 24 h after plating and coincides with the maximum levels of glutathione in the cells. When cells are treated with buthionine sulfoximine, which decreases glutathione levels in cells, telomerase activity decreases by 60%, and cell growth is delayed. Glutathione depletion in…

TelomeraseAntioxidantCell cycle checkpointTime FactorsCell divisionmedicine.medical_treatmentBlotting WesternImmunoblottingE2F4 Transcription FactorBiochemistryGene Expression Regulation Enzymologicchemistry.chemical_compoundMicemedicineAnimalsButhionine sulfoximineColoring AgentsMolecular BiologyButhionine SulfoximineTelomeraseInhibitor of Differentiation Protein 2Cell growthCell CycleCell BiologyGlutathione3T3 CellsTrypan BlueCell cycleFibroblastsFlow CytometryMolecular biologyGlutathioneDNA-Binding ProteinsRepressor ProteinschemistryOxidation-ReductionCell DivisionTranscription FactorsThe Journal of biological chemistry
researchProduct

No evidence for sequences structurally related to the RB1 gene in the human genome.

1991

The retinoblastoma (RB1) gene is a ubiquitously expressed gene encoding a cell-cycle control protein. Inactivation of this gene plays a crucial role in the development of retinoblastoma, osteosarcoma, and other tumors. In a search for structurally related gene sequences we identified a 5.5-kb BamHI fragment strongly cross-hybridizing with the 5′ end of the RB1 cDNA. Molecular cloning, in situ hybridization, restriction mapping, and sequence analysis identified this DNA segment as the 28S rRNA gene. The absence of other cross-hybridizing sequences suggests that the RB1 gene is not part of a structurally related gene family.

Therapeutic gene modulationGeneticsBase SequenceGenome HumanMolecular Sequence DataRestriction MappingPair-rule geneGene targetingBiologyDNA Ribosomaleye diseasesGene productBlotting SouthernGene mappingSequence Homology Nucleic AcidGene clusterRNA Ribosomal 28SGeneticsGene familyHumansGenes RetinoblastomaGenetics (clinical)Regulator geneHuman genetics
researchProduct

Dimerization of visinin-like protein 1 is regulated by oxidative stress and calcium and is a pathological hallmark of amyotrophic lateral sclerosis

2014

AbstractRedox control of proteins that form disulfide bonds upon oxidative challenge is an emerging topic in the physiological and pathophysiological regulation of protein function. We have investigated the role of the neuronal calcium sensor protein visinin-like protein 1 (VILIP-1) as a novel redox sensor in a cellular system. We have found oxidative stress to trigger dimerization of VILIP-1 within a cellular environment and identified thioredoxin reductase as responsible for facilitating the remonomerization of the dimeric protein. Dimerization is modulated by calcium and not dependent on the myristoylation of VILIP-1. Furthermore, we show by site-directed mutagenesis that dimerization is…

Thioredoxin reductaseAmino Acid MotifsBlotting Westernchemistry.chemical_elementMice TransgenicFree radicalsOxidative phosphorylationCalciumProtein aggregationmedicine.disease_causeBiochemistryMass SpectrometryMicechemistry.chemical_compoundSuperoxide Dismutase-1BAPTAPhysiology (medical)VILIP-1medicineAnimalsHumansCysteineMyristoylationSuperoxide DismutaseChemistryHEK 293 cellsAmyotrophic lateral sclerosisRedox sensorImmunohistochemistryCell biologyDisease Models AnimalOxidative StressHEK293 CellsBiochemistryNeurocalcinMutagenesis Site-DirectedCalciumProtein MultimerizationOxidation-ReductionOxidative stressFree Radical Biology and Medicine
researchProduct

A G468-T AMPD1 mutant allele contributes to the high incidence of myoadenylate deaminase deficiency in the Caucasian population.

2002

Myoadenylate deaminase deficiency is the most common metabolic disorder of skeletal muscle in the Caucasian population, affecting approximately 2% of all individuals. Although most deficient subjects are asymptomatic, some suffer from exercise-induced myalgia suggesting a causal relationship between a lack of enzyme activity and muscle function. In addition, carriers of this derangement in purine nucleotide catabolism may have an adaptive advantage related to clinical outcome in heart disease. The molecular basis of myoadenylate deaminase deficiency in Caucasians has been attributed to a single mutant allele characterized by double C to T transitions at nucleotides +34 and +143 in mRNA enco…

ThreonineDNA ComplementaryGenotypeBlotting WesternGlycineMetabolic myopathyBiologyCompound heterozygosityPolymerase Chain ReactionWhite PeopleAMP DeaminaseMetabolic DiseasesMuscular DiseasesGenotypemedicineHumansAlleleTransversionMuscle SkeletalGenetics (clinical)AllelesElectromyographyPoint mutationMetabolic disorderAMP deaminasemedicine.diseaseMolecular biologyPhenotypeNeurologyPediatrics Perinatology and Child HealthMutationNeurology (clinical)DNA ProbesNeuromuscular disorders : NMD
researchProduct