Search results for "toxin"

showing 10 items of 1434 documents

Study of the cytolethal distending toxin (CDT)-activated cell cycle checkpoint. Involvement of the CHK2 kinase.

2001

AbstractThe bacterial cytolethal distending toxin (CDT) triggers a G2/M cell cycle arrest in eukaryotic cells by inhibiting the CDC25C phosphatase-dependent CDK1 dephosphorylation and activation. We report that upon CDT treatment CDC25C is fully sequestered in the cytoplasmic compartment, an effect that is reminiscent of DNA damage-dependent checkpoint activation. We show that the checkpoint kinase CHK2, an upstream regulator of CDC25C, is phosphorylated and activated after CDT treatment. In contrast to what is observed with other DNA damaging agents, we demonstrate that the activation of CHK2 can only take place during S-phase. Use of wortmannin and caffeine suggests that this effect is no…

Intracellular FluidCell cycle checkpointCytolethal distending toxinCell Cycle ProteinsAtaxia Telangiectasia Mutated ProteinsBiochemistryS PhaseWortmanninchemistry.chemical_compoundStructural BiologyPhosphorylation0303 health sciences030302 biochemistry & molecular biologyCell CycleCell cycleProtein-Tyrosine Kinases3. Good healthCell biologyDNA-Binding Proteinsbiological phenomena cell phenomena and immunityWortmanninG2 PhaseCytolethal distending toxinBacterial ToxinsProto-Oncogene Proteins pp60(c-src)Biophysics[SDV.BC]Life Sciences [q-bio]/Cellular BiologyBiologyProtein Serine-Threonine KinasesCell Line03 medical and health sciencesCaffeineGeneticsHumanscdc25 PhosphatasesCHEK1Molecular Biology[SDV.BC] Life Sciences [q-bio]/Cellular Biology030304 developmental biologyCheckpoint 2 kinaseCyclin-dependent kinase 1Cell growthTumor Suppressor ProteinsCell BiologyG2-M DNA damage checkpointCDC25CAndrostadienesGenes cdcchemistryCancer researchHeLa CellsFEBS letters
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Intracellular Na+ concentration influences short-term plasticity of glutamate transporter-mediated currents in neocortical astrocytes.

2012

Fast synaptic transmission requires a rapid clearance of the released neurotransmitter from the extracellular space. Glial glutamate transporters (excitatory amino acid transporters, EAATs) strongly contribute to glutamate removal. In this work, we investigated the paired-pulse plasticity of synaptically activated, glutamate transporter-mediated currents (STCs) in cortical layer 2/3 astrocytes. STCs were elicited by local electrical stimulation in layer 4 in the presence of ionotropic glutamate (AMPA and NMDA), GABAA, and GABAB receptor antagonists. In experiments with low [Na+]i (5 mM) intrapipette solution, STCs elicited by paired-pulse stimulation demonstrated paired-pulse facilitation (…

Intracellular FluidPatch-Clamp TechniquesAmino Acid Transport System X-AGBiophysicsNipecotic AcidsAction PotentialsNeocortexAMPA receptorTetrodotoxinBiologyGABAB receptorAnisolesIn Vitro TechniquesSynaptic TransmissionGABA AntagonistsCellular and Molecular NeuroscienceMiceCadmium ChlorideEthers CyclicOximesmedicineGABA transporterAnimalsgamma-Aminobutyric AcidBenzofuransAspartic AcidNeuronal PlasticityGABAA receptorRhodaminesSodiumGlutamate receptorCalcium Channel BlockersElectric StimulationMice Inbred C57BLmedicine.anatomical_structureNeurologyAnimals NewbornAstrocytesExcitatory postsynaptic potentialBiophysicsbiology.proteinNMDA receptorNeuroscienceExcitatory Amino Acid AntagonistsAstrocyteSodium Channel BlockersGlia
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Gabapentin in the treatment of hemifacial spasm

2001

Objectives To evaluate the efficacy of gabapentin in the treatment of hemifacial spasm. Material and methods Twenty-three patients with hemifacial spasm not suitable for surgery or therapy with botulinum toxin were treated with gabapentin. The main efficacy parameter was the percentage of spasm reduction. Results A clinically significant reduction of spasms was obtained by 16 patients. Conclusion Gabapentin was effective and safe in reducing hemifacial spasm in 16 out 23 (69.6%) patients.

Involuntary movementChemotherapymedicine.medical_specialtyGabapentinbusiness.industrymedicine.medical_treatmentTreatment outcomeGeneral Medicinemedicine.diseaseBotulinum toxinnervous system diseasesSurgerybody regionsClinical trialstomatognathic diseasesAnticonvulsantNeurologyAnesthesiaotorhinolaryngologic diseasesMedicinecardiovascular diseasesNeurology (clinical)businessHemifacial spasmmedicine.drugActa Neurologica Scandinavica
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Dispersive magnetic immunoaffinity extraction. Anatoxin-a determination.

2017

Specific monoclonal antibodies were coupled with magnetic Sepharose-based beads and used, for the first time. The methodology was applied to preconcentrate anatoxin-a from water and the later determination by ion mobility spectrometry (IMS). Dispersive magnetic immunoaffinity (d-MagIA) extraction methodology provided a limit of detection of 0.02μgL-1 and a satisfactory precision with a relative standard deviation lower than 15%. Recoveries were evaluated at 0.5, 1.0 and 5.0μgL-1 anatoxin-a with quantitative values from 91 to 115%. Additionally, isobaric interferences with phenylalanine were completely avoided by the use of the developed d-MagIA extraction coupled to IMS determinations.

Ion-mobility spectrometryRelative standard deviationAnalytical chemistry02 engineering and technology01 natural sciencesBiochemistryAnalytical ChemistryAnatoxin-aSepharosechemistry.chemical_compoundMagneticsLimit of DetectionIon Mobility SpectrometryDetection limitChromatographyCyanobacteria ToxinsSepharose010401 analytical chemistryOrganic ChemistryExtraction (chemistry)Antibodies MonoclonalWaterGeneral Medicine021001 nanoscience & nanotechnology0104 chemical scienceschemistryIsobaric process0210 nano-technologyWater Pollutants ChemicalEnvironmental MonitoringTropanesJournal of chromatography. A
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Resealing of large transmembrane pores produced by streptolysin O in nucleated cells is accompanied by NF‐κB activation and downstream events

2001

Streptolysin O (SLO), archetype of a cholesterol-binding bacterial cytolysin, forms large pores in the plasma membrane of mammalian cells. We have recently reported that when a limited number of pores are generated in a cell, they can be sealed in a Ca++-dependent process. Here, we show that resealing is followed by the release of IL-6 and IL-8 from keratinocytes and from endothelial cells, both relevant targets for SLO attack. Production of cytokines by these cells was preceded by activation of transcription factor nuclear factor kappaB, which thus emerges as a common denominator of stress responses to various pore-forming agents, including alpha-toxin of Staphylococcus aureus and compleme…

KeratinocytesCell Membrane PermeabilityTime FactorsBiologyBiochemistryCell LineAdenosine TriphosphateBacterial ProteinsNucleated cellGeneticsHumansInterleukin 8Molecular BiologyMicrobial toxinsMembrane permeabilizationDose-Response Relationship Drugintegumentary systemInterleukin-6Interleukin-8NF-kappa BTransmembrane proteinCell biologyStreptolysinsStreptolysinEndothelium VascularNf κb activationBiotechnologyThe FASEB Journal
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Genetic ablation of mast cells redefines the role of mast cells in skin wound healing and bleomycin-induced fibrosis.

2014

Conclusive evidence for the impact of mast cells (MCs) in skin repair is still lacking. Studies in mice examining the role of MC function in the physiology and pathology of skin regenerative processes have obtained contradictory results. To clarify the specific role of MCs in regenerative conditions, here we used a recently developed genetic mouse model that allows conditional MC ablation to examine MC-specific functions in skin. This mouse model is based on the cell type–specific expression of Cre recombinase in connective tissue–type MCs under control of the Mcpt5 promoter and the Cre-inducible diphtheria toxin receptor–mediated cell lineage ablation by diphtheria toxin. In response to ex…

KeratinocytesPathologymedicine.medical_specialtymedicine.medical_treatmentCellCre recombinaseMice TransgenicDermatologyBiologyBleomycinBiochemistrySkin Diseaseschemistry.chemical_compoundBleomycinMiceFibrosismedicineLeukocytesAnimalsMast CellsMolecular BiologyDiphtheria toxinSkin repairWound HealingAntibiotics AntineoplasticGranulation tissueCell BiologyAblationmedicine.diseaseFibrosisDisease Models Animalmedicine.anatomical_structurechemistryGranulation TissueThe Journal of investigative dermatology
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Differential role of p38 mitogen activated protein kinase for cellular recovery from attack by pore-forming S. aureus alpha-toxin or streptolysin O.

2006

Following the observation that cells are able to recover from membrane lesions incurred by Staphylococcus aureus alpha-toxin and streptolysin O (SLO), we investigated the role of p38 in this process. p38 phosphorylation occurred in response to attack by both toxins, commencing within minutes after toxin treatment and waning after several hours. While SLO reportedly activates p38 via ASK1 and ROS, we show that this pathway does not play a major role for p38 induction in alpha-toxin-treated cells. Strikingly divergent effects of p38 blockade were noted depending on the toxin employed. In the case of alpha-toxin, inhibition of p38 within the time frame of its activation led to disruption of th…

KeratinocytesProgrammed cell deathStaphylococcus aureusCell Membrane Permeabilityp38 mitogen-activated protein kinasesBacterial ToxinsBiophysicsBiologymedicine.disease_causeMAP Kinase Kinase Kinase 5Biochemistryp38 Mitogen-Activated Protein KinasesMicrobiologyHemolysin ProteinsAdenosine TriphosphateBacterial ProteinsProto-Oncogene ProteinsmedicineHumansASK1PhosphorylationMolecular BiologyCells CulturedPore-forming toxinToxinCell MembraneCell BiologyProtein-Tyrosine KinasesBlockadeCell biologyEnzyme ActivationStreptolysinsPhosphorylationStreptolysinBiochemical and biophysical research communications
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Staphylococcal alpha-toxin kills human keratinocytes by permeabilizing the plasma membrane for monovalent ions

1993

Incubation of human keratinocytes with nanomolar concentrations of Staphylococcus aureus alpha-toxin leads to irreversible depletion of cellular ATP. The toxin forms hexamers in the target cell membranes, and rapid transmembrane flux of K+, Na+, and 86Rb+ is observed. Unexpectedly, pores formed in keratinocytes through application of low but lethal doses of alpha-toxin appeared to be considerably smaller than those formed in erythrocyte membranes. They permitted neither rapid influx of Ca2+ or propidium iodide, nor efflux of carboxyfluorescein. Larger pores allowing flux of all three markers did form when the toxin was applied at high concentrations. Flux of monovalent ions and reduction in…

KeratinocytesStaphylococcus aureusCell Membrane PermeabilityBacterial ToxinsImmunologyMolecular ConformationBiologymedicine.disease_causeMicrobiologyCell membraneHemolysin Proteinschemistry.chemical_compoundOxygen ConsumptionNucleated cellmedicineExtracellularHumansPropidium iodideCells CulturedCell DeathToxinCell MembraneCations MonovalentCulture MediaMolecular WeightKineticsCytolysisInfectious Diseasesmedicine.anatomical_structureMembraneBiochemistrychemistryPotassiumBiophysicsCalciumParasitologyFlux (metabolism)Research ArticleInfection and Immunity
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Pore-forming Staphylococcus aureus alpha-toxin triggers epidermal growth factor receptor-dependent proliferation.

2006

Staphylococcal alpha-toxin is an archetypal killer protein that homo-oligomerizes in target cells to create small transmembrane pores. The membrane-perforating beta-barrel motif is a conserved attack element of cytolysins of Gram-positive and Gram-negative bacteria. Following the recognition that nucleated cells can survive membrane permeabilization, a profile of abundant transcripts was obtained in transiently perforated keratinocytes. Several immediate early genes were found to be upregulated, reminiscent of the cellular response to growth factors. Cell cycle analyses revealed doubling of S + G2/M phase cells 26 h post toxin treatment. Determination of cell counts uncovered that after an …

KeratinocytesStaphylococcus aureusSrc Homology 2 Domain-Containing Transforming Protein 1ImmunologyCellBacterial ToxinsBlotting WesternFluorescent Antibody TechniqueTransfectionMicrobiologyCell LineHemolysin ProteinsDownregulation and upregulationNucleated cellVirologymedicineHumansGrowth factor receptor inhibitorEpidermal growth factor receptorStaphylococcus aureus alpha toxinAdaptor Proteins Signal TransducingCell Line TransformedCell ProliferationbiologyCytotoxinsReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCell CycleCell cycleFlow CytometryTransmembrane proteinCell biologyErbB Receptorsmedicine.anatomical_structureShc Signaling Adaptor Proteinsbiology.proteinMitogensSignal TransductionCellular microbiology
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Endotoxins in ophthalmic viscosurgical devices.

2003

Purpose To measure the endotoxin concentration (EC) of 25 commercially available, hyaluronic acid- and hydroxypropylmethylcellulose-based (HPMC) ophthalmic viscosurgical devices (OVDs). Methods The in vitro Limulus amebocyte lysate (LAL) assay, which indicates the presence of endotoxins originating from gram-negative bacteria, was used to determine the EC. The procedure was performed according to the European Pharmacopoeia/USP. EC including duplicate determinations, negative controls, dilution series with control standard endotoxin, dilution series with sample extract and positive sample control. Results 16 OVDs (Amvisc®, Amvisc® Plus, Biolon®, Coatel®, Healon®, Healon® GV, Healon®5, HPMC O…

LactoseLimulus testOphthalmologic Surgical ProceduresMethylcelluloseSensitivity and Specificity03 medical and health sciences0302 clinical medicineGram-Negative BacteriaOxazinesHumansConcentration factorHyaluronic AcidLimulus TestEndophthalmitisChromatographyPositive sampleChemistryReproducibility of ResultsGeneral MedicineDilutionEndotoxinsOphthalmologyLimulus amebocyte lysateImmunology030221 ophthalmology & optometry030217 neurology & neurosurgery
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