Search results for "Diphtheria Toxin"

showing 5 items of 15 documents

Comparative effects of carrier proteins on vaccine-induced immune response

2011

The efficacy of vaccines against major encapsulated bacterial pathogens -Neisseria meningitidis, Streptococcus pneumoniae, and Haemophilus influenzae type b (Hib) - has been significantly enhanced by conjugating the respective polysaccharides with different carrier proteins: diphtheria toxoid; non-toxic cross-reactive material of diphtheria toxin(197), tetanus toxoid, N. meningitidis outer membrane protein, and non-typeable H. influenzae-derived protein D. Hib, meningococcal, and pneumococcal conjugate vaccines have shown good safety and immunogenicity profiles regardless of the carrier protein used, although data are conflicting as to which carrier protein is the most immunogenic. Coadmini…

Meningococcal Vaccineschemical and pharmacologic phenomenamedicine.disease_causecomplex mixturesMicrobiologyPneumococcal VaccinesImmune systemAdjuvants ImmunologicConjugate vaccineStreptococcus pneumoniaemedicineHumansHaemophilus VaccinesDiphtheria toxinVaccines ConjugateGeneral VeterinaryGeneral Immunology and MicrobiologyChemistryNeisseria meningitidisImmunogenicityPolysaccharides BacterialPublic Health Environmental and Occupational HealthToxoidVaccine efficacyVirologyInfectious DiseasesMolecular MedicineCarrier ProteinsVaccine
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Killer-toxin-resistant kre12 mutants of Saccharomyces cerevisiae: genetic and biochemical evidence for a secondary K1 membrane receptor.

1995

The Saccharomyces cerevisiae killer toxin K1 is a secreted alpha/beta-heterodimeric protein toxin that kills sensitive yeast cells in a receptor-mediated two-stage process. The first step involves toxin binding to beta-1,6-D-glucan-components of the outer yeast cell surface; this step is blocked in yeast mutants bearing nuclear mutations in any of the KRE genes whose products are involved in synthesis and/or assembly of cell wall beta-D-glucans. After binding to the yeast cell wall, the killer toxin is transferred to the cytoplasmic membrane, subsequently leading to cell death by forming lethal ion channels. In an attempt to identify a secondary K1 toxin receptor at the plasma membrane leve…

MutantSaccharomyces cerevisiaeGenes FungalReceptors Cell SurfaceSaccharomyces cerevisiaeSpheroplastsBiologymedicine.disease_causeBiochemistryMicrobiologyModels BiologicalIon ChannelsFungal ProteinsCell surface receptorCell WallGeneticsmedicineMolecular BiologyDiphtheria toxinToxinMembrane ProteinsDrug Resistance MicrobialGeneral MedicineSpheroplastMycotoxinsbiology.organism_classificationYeastKiller Factors YeastBiochemistryMembrane proteinMutationArchives of microbiology
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D2R striatopallidal neurons inhibit both locomotor and drug reward processes.

2009

The specific functions of dopamine D(2) receptor-positive (D(2)R) striatopallidal neurons remain poorly understood. Using a genetic mouse model, we found that ablation of D(2)R neurons in the entire striatum induced hyperlocomotion, whereas ablation in the ventral striatum increased amphetamine conditioned place preference. Thus D(2)R striatopallidal neurons limit both locomotion and, unexpectedly, drug reinforcement.

Time FactorsstriatumParkinson's diseaseStriatumNeurons -- drug effectsEnkephalins -- metabolism10263 Institute of Experimental ImmunologyMiceDopamine Uptake InhibitorsTyrosine 3-Monooxygenase -- geneticsCorpus Striatum -- cytologyDiphtheria ToxinGlutamate Decarboxylase -- metabolismstriatum; indirect opathway; A2A receptors; D2 receptors; locomotion; amphetamine addiction; Parkinson's diseaseNeuronsamphetamine addictionGlutamate DecarboxylaseGeneral NeuroscienceAmphetamine -- pharmacologyNeurodegeneration2800 General NeuroscienceEnkephalinsSciences bio-médicales et agricoleslocomotionmedicine.anatomical_structureA2A receptorsIntercellular Signaling Peptides and ProteinsReceptors Dopamine D2 -- metabolismPsychologyLocomotionmedicine.drugHeparin-binding EGF-like Growth FactorProtein BindingGlobus Pallidus -- cytologyReceptors Dopamine D2 -- deficiencyReinforcement ScheduleTyrosine 3-MonooxygenaseGlutamate Decarboxylase -- geneticsLocomotion -- geneticsIntercellular Signaling Peptides and Proteins -- genetics610 Medicine & healthMice TransgenicNerve Tissue ProteinsDiphtheria Toxin -- pharmacologyGlobus PallidusNeurons -- physiologyLocomotion -- drug effectsRewardDopamineDopamine receptor D2medicineNerve Tissue Proteins -- metabolismAnimalsGene Expression Regulation -- geneticsAmphetamineD2 receptorsReceptors Adenosine A2Receptors Dopamine D2indirect opathwayVentral striatumReceptors Adenosine A2 -- geneticsDopamine Uptake Inhibitors -- pharmacologymedicine.diseaseConditioned place preferenceCorpus StriatumMice Inbred C57BLGene Expression Regulation -- drug effectsAmphetaminenervous systemGene Expression RegulationProtein Binding -- drug effectsTyrosine 3-Monooxygenase -- metabolism570 Life sciences; biologyAutoradiographyConditioning OperantNeuronConditioning Operant -- physiologyNeuroscienceEnkephalins -- geneticsNature neuroscience
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Acute selective ablation of rat insulin promoter-expressing (RIP HER ) neurons defines their orexigenic nature

2012

Rat insulin promoter (RIP)-expressing neurons in the hypothalamus control body weight and energy homeostasis. However, genetic approaches to study the role of these neurons have been limited by the fact that RIP expression is predominantly found in pancreatic β-cells, which impedes selective targeting of neurons. To define the function of hypothalamic RIP-expressing neurons, we set out to acutely and selectively eliminate them via diphtheria toxin-mediated ablation. Therefore, the diphtheria toxin receptor transgene was specifically expressed upon RIP-specific Cre recombination using a RIP-Cre line first described by Herrera (RIP HER -Cre) [Herrera PL (2000) Development 127:2317–2322]. Usi…

endocrine systemmedicine.medical_specialtyPituitary glandBiologyReal-Time Polymerase Chain ReactionEnergy homeostasisMiceArcuate nucleusOrexigenicInternal medicineWeight LossmedicineAnimalsInsulinPromoter Regions GeneticDorsomedial hypothalamic nucleusNeuronsDiphtheria toxinMultidisciplinarydigestive oral and skin physiologyArcuate Nucleus of HypothalamusFeeding BehaviorBiological SciencesGlucose Tolerance TestRatsEndocrinologymedicine.anatomical_structurenervous systemHypothalamusNucleushormones hormone substitutes and hormone antagonistsParaventricular Hypothalamic Nucleusmedicine.drugProceedings of the National Academy of Sciences
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Agouti-related peptide-expressing neurons are mandatory for feeding.

2005

Multiple hormones controlling energy homeostasis regulate the expression of neuropeptide Y (NPY) and agouti-related peptide (AgRP) in the arcuate nucleus of the hypothalamus. Nevertheless, inactivation of the genes encoding NPY and/or AgRP has no impact on food intake in mice. Here we demonstrate that induced selective ablation of AgRP-expressing neurons in adult mice results in acute reduction of feeding, demonstrating direct evidence for a critical role of these neurons in the regulation of energy homeostasis.

medicine.medical_specialtyPro-OpiomelanocortinTime FactorsPeptideCell CountBiologyEnergy homeostasisEatingMiceArcuate nucleusInternal medicinemedicineAnimalsAgouti-Related ProteinDiphtheria ToxinNeuropeptide YRegulation of gene expressionchemistry.chemical_classificationMice KnockoutNeuronsGeneral Neurosciencedigestive oral and skin physiologyBody WeightArcuate Nucleus of HypothalamusProteinsFeeding BehaviorNeuropeptide Y receptorbeta-GalactosidaseAnorexiaEndocrinologynervous systemchemistryGene Expression RegulationHypothalamusIntercellular Signaling Peptides and ProteinsAgouti-related peptidehormones hormone substitutes and hormone antagonistsHormoneNature neuroscience
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