Search results for "Sulfur Radioisotopes"

showing 7 items of 7 documents

Altered atypical coupling of γ-aminobutyrate type A receptor agonist and convulsant binding sites in subunit-deficient mouse lines

2001

We searched for subunit correlations for GABA(A) receptor-associated atypically GABA-insensitive [35S]TBPS binding. The homomeric beta3 subunit receptors could be excluded, as GABA-insensitive [35S]TBPS binding was present in beta3-/- mice. Localization of GABA-insensitive [35S]TBPS binding correlated best with those of delta, alpha4 and alpha6 subunit mRNAs. The amounts of GABA-insensitive [35S]TBPS binding components were increased in delta-/- mice, but dramatically reduced in alpha6-/- mice, suggesting a role for alpha6 but excluding delta subunits.

Agonistmedicine.medical_specialtymedicine.drug_classProtein subunitMolecular Sequence DataConvulsantsBiologySulfur Radioisotopesmedicine.disease_causeMiceRadioligand AssayCellular and Molecular NeuroscienceInternal medicinemedicineAnimalsHomomericRNA MessengerBinding siteReceptorGABA AgonistsMolecular BiologyBrain ChemistryMice KnockoutMutationBinding SitesGABAA receptorBridged Bicyclo Compounds HeterocyclicReceptors GABA-AMolecular biologyEndocrinologynervous systemConvulsantMolecular Brain Research
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Characterization of γ-aminobutyrate type A receptors with atypical coupling between agonist and convulsant binding sites in discrete brain regions

2001

Abstract γ-Aminobutyric acid type A (GABA A ) receptor ionophore ligand t -[ 35 S]butylbicyclophosphorothionate ([ 35 S]TBPS) was used in an autoradiographic assay on brain cryostat sections to visualize and characterize atypical GABA-insensitive [ 35 S]TBPS binding previously described in certain recombinant GABA A receptors and the cerebellar granule cell layer. Picrotoxinin-sensitive but 1-mM GABA-insensitive [ 35 S]TBPS binding was present in the rat cerebellar granule cell layer, many thalamic nuclei, subiculum and the internal rim of the cerebral cortex, amounting in these regions up to 6% of the basal binding determined in the absence of exogenous GABA. Similar binding properties wer…

MaleAgonistAzidesmedicine.medical_specialtyCerebellumSesterterpenesmedicine.drug_classLoreclezoleConvulsantsBiologySulfur RadioisotopesTritiumBinding CompetitiveBenzodiazepinesRadioligand AssayCellular and Molecular Neurosciencechemistry.chemical_compoundThalamusCerebellumInternal medicinemedicineAnimalsHumansPicrotoxinRats WistarBinding siteReceptorGABA AgonistsMolecular Biologygamma-Aminobutyric AcidMuscimolGABAA receptorAffinity LabelsBridged Bicyclo Compounds HeterocyclicReceptors GABA-AGranule cellRatsEndocrinologymedicine.anatomical_structurenervous systemMuscimolchemistryBiophysicsChickensmedicine.drugMolecular Brain Research
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Complement C1q is dramatically up-regulated in brain microglia in response to transient global cerebral ischemia.

2000

Abstract Recent evidence suggests that the pathophysiology of neurodegenerative and inflammatory neurological diseases has a neuroimmunological component involving complement, an innate humoral immune defense system. The present study demonstrates the effects of experimentally induced global ischemia on the biosynthesis of C1q, the recognition subcomponent of the classical complement activation pathway, in the CNS. Using semiquantitative in situ hybridization, immunohistochemistry, and confocal laser scanning microscopy, a dramatic and widespread increase of C1q biosynthesis in rat brain microglia (but not in astrocytes or neurons) within 24 h after the ischemic insult was observed. A marke…

MaleImmunologyIschemiaInflammationIn situ hybridizationBiologySulfur RadioisotopesProinflammatory cytokineRNA ComplementaryCerebrospinal fluidDownregulation and upregulationmedicineImmunology and AllergyAnimalsTransient (computer programming)Rats WistarComplement C1qIn Situ HybridizationPharmacologyMicrogliaComplement C1qBrainRNA Probesmedicine.diseaseImmunohistochemistryCell biologyComplement systemRatsUp-Regulationmedicine.anatomical_structureIschemic Attack TransientImmunologyMicrogliamedicine.symptomNeuroscienceDigoxigeninJournal of immunology (Baltimore, Md. : 1950)
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In human and rat lung membranes [35s]GTPγS binding is a tool for pharmacological characterization of G protein-coupled devucleotide receptors

1999

The P2Y receptor family is activated by extracellular nucleotides such as ATP and UTP. P2Y receptors regulate physiological functions in numerous cell types. In lung, the P2Y2 receptor subtype plays a role in controlling Cl- and fluid transport. Besides ATP or UTP, also diadenosine tetraphosphate (Ap4A), a stable nucleotide, seems to be of physiological importance. In membrane preparations from human and rat lung we applied several diadenosine polyphosphates to investigate whether they act as agonists for G protein-coupled receptors. We assessed this by determining the stimulation of [35S]GTPgammaS binding. Stimulation of [35S]GTPgammaS binding to G proteins has already been successfully ap…

P2Y receptorG proteinGTPgammaSReceptors Cell SurfaceBiologySulfur RadioisotopesGeneral Biochemistry Genetics and Molecular BiologyRadioligand Assaychemistry.chemical_compoundSpecies SpecificityGTP-Binding ProteinsAnimalsHumansGeneral Pharmacology Toxicology and PharmaceuticsReceptorLungG protein-coupled receptorG protein-coupled receptor kinaseMembranesReceptors Purinergic P2General MedicineFluid transportRatschemistryBiochemistryGuanosine 5'-O-(3-Thiotriphosphate)Ap4ALife Sciences
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Expression of the human complement C8 subunits is independently regulated by interleukin 1β, interleukin 6, and interferon γ

1998

The eighth component of human complement (C8) is composed of two subunits which are products from three separate genes. The alpha-gamma- and the beta-subunit of C8 are expressed independently, and are part of the membrane attack complex. C8 is primarily synthesized in the liver. It has been shown in previous studies that the human hepatoma cell line HepG2 constitutively expresses C8, and thus is a suitable model system for studying C8 biosynthesis in vitro. Expression is modulated by the cytokines IL-1 beta, IL-6 and IFN-gamma. The effect of the different cytokines on the expression of these subunits was examined using biosynthetical labelling and immunoprecipitation methods. C8 alpha-gamma…

PharmacologybiologyInterleukin-6ImmunoprecipitationAntineoplastic AgentsSulfur RadioisotopesComplement C8Precipitin TestsMolecular biologyIn vitroComplement systemInterferon-gammaGene expressionTumor Cells Culturedbiology.proteinHumansSecretionInterleukin 6Beta (finance)Complement membrane attack complexInterleukin-1Immunopharmacology
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Dithiothreitol Treatment of Madin-Darby Canine Kidney Cells Reversibly Blocks Export from the Endoplasmic Reticulum but Does Not Affect Vectorial Tar…

1995

Addition of dithiothreitol (DTT) to the culture medium of Madin-Darby canine kidney (MDCK) cells blocks transport of newly synthesized gp80 (clusterin, apolipoprotein J), a soluble marker protein for apical exocytosis in this epithelial cell line. In cells treated with DTT during pulse labeling, gp80 is retained in the endoplasmic reticulum. After removal of the reducing agent, gp80 is posttranslationally oxidized and secreted at the apical surface of MDCK cell monolayers. This demonstrates that when folded and oxidized posttranslationally, gp80 can acquire a conformation that exhibits sorting signals for vectorial targeting. In the continuous presence of DTT, the transepithelial electrical…

Protein FoldingProtein ConformationBiologyEndoplasmic ReticulumKidneySulfur RadioisotopesBiochemistryEpitheliumExocytosisDithiothreitolCell LineMembrane Potentialssymbols.namesakechemistry.chemical_compoundDogsMethioninemedicineAnimalsCysteineSalivary Proteins and PeptidesMolecular BiologySecretory pathwayGlycoproteinsTight junctionEndoplasmic reticulumCell MembraneCell BiologyGolgi apparatusEpitheliumCell biologyDithiothreitolClusterinmedicine.anatomical_structureSecretory proteinchemistrysymbolsOxidation-ReductionProtein Processing Post-TranslationalMolecular ChaperonesJournal of Biological Chemistry
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Prenatal diagnosis of mucolipidosis II (I-cell disease)

1976

A pregnancy at risk for mucolipidosis II (I-cell disease) was monitored in which an affected fetus was predicted on the basis of the analyses of lysosomal hydrolases in amniotic fluid and cultured amniotic fluid cells, and by the demonstration of an excessive accumulation of [35S] sulfate-labeled glycosaminoglycans in cultured amniotic cells. This diagnosis was confirmed by performing enzyme assays and [35S] sulfate incorporation studies on material derived from the aborted fetus.

medicine.medical_specialtyAmniotic fluidHydrolasesPrenatal diagnosisSulfur RadioisotopesAndrologyGlycosaminoglycanPregnancyPrenatal DiagnosisInternal medicinemedicineHumansRadiology Nuclear Medicine and imagingCells CulturedGlycosaminoglycansPregnancyFetusbusiness.industryMucolipidosisAborted FetusGeneral MedicineMucopolysaccharidosesAmniotic Fluidmedicine.diseaseEndocrinologyPediatrics Perinatology and Child HealthFemaleI-cell diseaseLysosomesbusinessEuropean Journal of Pediatrics
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