2009
Maitotoxin converts the plasmalemmal Ca2+ pump into a Ca2+-permeable nonselective cation channel
Sinkins W, Estacion M, Prasad V, Goel M, Shull G, Kunze D, Schilling W. Maitotoxin converts the plasmalemmal Ca2+ pump into a Ca2+-permeable nonselective cation channel. American Journal Of Physiology - Cell Physiology 2009, 297: c1533-c1543. PMID: 19794142, PMCID: PMC2793065, DOI: 10.1152/ajpcell.00252.2009.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine TriphosphateAnimalsAnimals, Genetically ModifiedCalciumCation Transport ProteinsCationsCell MembraneCells, CulturedDown-RegulationElectric ConductivityFibroblastsHumansIon ChannelsKidneyMarine ToxinsMiceOxocinsPermeabilityPlasma Membrane Calcium-Transporting ATPasesRNA, Small InterferingSpodopteraUp-RegulationConceptsPermeable nonselective cation channelNonselective cation channelsCation channelsSpodoptera frugiperda (Sf9) insect cellsHEK cellsMouse embryonic fibroblastsHuman embryonic kidney 293 cellsEmbryonic kidney 293 cellsKidney 293 cellsInsect cellsEmbryonic fibroblastsWhole-cell membrane currentsMolecular identityCell membrane currentsCell typesPMCACytosolic freeMarine toxinsEnhanced expressionWhole-cell currentsPlasmalemmal Ca2PalytoxinATPaseCellsMaitotoxin
2004
Maitotoxin Induces Biphasic Interleukin-1β Secretion and Membrane Blebbing in Murine Macrophages
Verhoef P, Kertesy S, Estacion M, Schilling W, Dubyak G. Maitotoxin Induces Biphasic Interleukin-1β Secretion and Membrane Blebbing in Murine Macrophages. Molecular Pharmacology 2004, 66: 909-920. PMID: 15385641, DOI: 10.1124/mol.66.4.909.Peer-Reviewed Original ResearchConceptsMTX treatmentMIL-1betaIL-1betaCytolytic releaseProIL-1betaProinflammatory cytokine interleukin-1betaProinflammatory cytokine secretionCytokine interleukin-1betaMature IL-1betaMurine macrophagesInterleukin-1β secretionCytokine releaseInflammatory leukocytesCytokine secretionP2X7 receptorInterleukin-1betaInflammatory macrophagesExtracellular Ca2Extracellular glycineIntracellular Ca2Vivo responseMacrophagesCation channelsSecretionLytic phaseMaitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity
Wisnoskey B, Estacion M, Schilling W. Maitotoxin-induced cell death cascade in bovine aortic endothelial cells: divalent cation specificity and selectivity. American Journal Of Physiology - Cell Physiology 2004, 287: c345-c356. PMID: 15044153, DOI: 10.1152/ajpcell.00473.2003.Peer-Reviewed Original ResearchConceptsCell death cascadeSingle-cell levelBovine aortic endothelial cellsDeath cascadeMembrane blebsAortic endothelial cellsCell population levelGreen fluorescent proteinSubsequent cell lysisPlasmalemmal permeabilityCell demiseEndothelial cellsFluorescent proteinLarge proteinsCation specificityNonselective cation channelsProteinCation channelsLytic phaseCytosolic freeCell lysisPropidium iodidePopulation levelEthidium bromideCascadeActivation of Human TRPC6 Channels by Receptor Stimulation*
Estacion M, Li S, Sinkins W, Gosling M, Bahra P, Poll C, Westwick J, Schilling W. Activation of Human TRPC6 Channels by Receptor Stimulation*. Journal Of Biological Chemistry 2004, 279: 22047-22056. PMID: 15023993, DOI: 10.1074/jbc.m402320200.Peer-Reviewed Original ResearchMeSH KeywordsCalcium ChannelsCarbacholCell LineCell MembraneCholinergic AgonistsDNA, ComplementaryDose-Response Relationship, DrugElectrophysiologyEnzyme InhibitorsHumansIonomycinIonophoresKineticsLac OperonMembrane PotentialsProtein BindingTetradecanoylphorbol AcetateThapsigarginTime FactorsTransfectionTRPC Cation ChannelsTRPC6 Cation ChannelConceptsReceptor stimulationTRPC6 currentsTRPC6 channelsSteep dose-response relationshipEffect of carbacholConcentrations of carbacholSteep concentration-response relationshipReceptor-mediated eventsActivation of TRPC6Channel activityDose-response relationshipWhole-cell membrane currentsSignificant acute effectConcentration-response relationshipCell membrane currentsAcute effectsCarbacholGeneration of DAGHuman embryonic kidney cellsPrior stimulationPatch pipetteTRPC6 activityEmbryonic kidney cellsMembrane currentsMembrane depolarization
2002
Blockade of maitotoxin-induced oncotic cell death reveals zeiosis
Estacion M, Schilling W. Blockade of maitotoxin-induced oncotic cell death reveals zeiosis. BMC Physiology 2002, 2: 2. PMID: 11825342, PMCID: PMC65053, DOI: 10.1186/1472-6793-2-2.Peer-Reviewed Original Research
2001
Maitotoxin-induced membrane blebbing and cell death in bovine aortic endothelial cells
Estacion M, Schilling W. Maitotoxin-induced membrane blebbing and cell death in bovine aortic endothelial cells. BMC Physiology 2001, 1: 2. PMID: 11231888, PMCID: PMC32181, DOI: 10.1186/1472-6793-1-2.Peer-Reviewed Original Research
1993
Competence induction by PDGF requires sustained calcium influx by a mechanism distinct from storage-dependent calcium influx
Estacion M, Mordan L. Competence induction by PDGF requires sustained calcium influx by a mechanism distinct from storage-dependent calcium influx. Cell Calcium 1993, 14: 439-454. PMID: 8395338, DOI: 10.1016/0143-4160(93)90003-o.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBucladesineCalciumCalcium ChannelsCell CompartmentationCell DivisionCell LineCell MembraneColforsinContact InhibitionDNA ReplicationDrug SynergismExtracellular SpaceFibroblastsGallic AcidInsulinIon Channel GatingLanthanumMiceMice, Inbred C3HNifedipinePlatelet-Derived Growth FactorS PhaseSignal TransductionTetradecanoylphorbol AcetateConceptsCalcium influxIntracellular storage sitesExtracellular calciumCalcium influx pathwaySustained calcium influxIntracellular calcium concentrationExtracellular calcium influxRelease of calciumPercentage of cellsC3H 10T1/2 mouse fibroblastsPDGF exposureSustained elevationTMB-8Influx pathwayBiphasic increaseSustained increaseDibutyryl cGMPCalcium concentrationS phasePDGFDibutyryl cAMPCell replicationSelective inhibitionReplicative competenceProgression