2025
α-Latrotoxin Actions in the Absence of Extracellular Ca2+ Require Release of Stored Ca2+
Blackburn J, Islam Q, Benlaouer O, Tonevitskaya S, Petitto E, Ushkaryov Y. α-Latrotoxin Actions in the Absence of Extracellular Ca2+ Require Release of Stored Ca2+. Toxins 2025, 17: 73. PMID: 39998090, PMCID: PMC11860464, DOI: 10.3390/toxins17020073.Peer-Reviewed Original ResearchConceptsAbsence of extracellular Ca<sup>2+</sup> anRelease of stored Ca2+Store-operated Ca<sup>2+</sup> entryExtracellular Ca<sup>2+</sup>Absence of extracellular Ca2Nerve terminalsCytosolic Ca<sup>2+</sup>Neurotransmitter releaseOpening of Ca<sup>2+</sup> channelsControl of neurotransmitter releaseRelease of neurotransmittersIntracellular storesExtracellular Ca2BAPTA-AMG protein-coupled receptorsMouse neuromuscular junctionCation ionophoreSensitive to inhibitorsCa2+Neuromuscular junctionNerveNeurotransmitterPhysiological controlReleaseInflux
2018
Polycystin-2-dependent control of cardiomyocyte autophagy
Criollo A, Altamirano F, Pedrozo Z, Schiattarella GG, Li DL, Rivera-Mejías P, Sotomayor-Flores C, Parra V, Villalobos E, Battiprolu PK, Jiang N, May HI, Morselli E, Somlo S, de Smedt H, Gillette TG, Lavandero S, Hill JA. Polycystin-2-dependent control of cardiomyocyte autophagy. Journal Of Molecular And Cellular Cardiology 2018, 118: 110-121. PMID: 29518398, DOI: 10.1016/j.yjmcc.2018.03.002.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseIntracellular CaCardiomyocyte autophagyAutophagic fluxBAPTA-AMDominant polycystic kidney diseaseStress-induced autophagySarcoplasmic reticulum CaPolycystic kidney diseasePolycystin-2Impaired autophagic fluxKidney diseaseKnockout miceConsiderable evidence pointsMTOR inhibitionReticulum CaExtracellular CaMultiple cell typesAutophagic activityAutophagy inductionHomeostasisAutophagyEvidence pointsAutophagic controlCell types
2015
Regulation of glomerulotubular balance. III. Implication of cytosolic calcium in flow-dependent proximal tubule transport
Du Z, Weinbaum S, Weinstein A, Wang T. Regulation of glomerulotubular balance. III. Implication of cytosolic calcium in flow-dependent proximal tubule transport. American Journal Of Physiology. Renal Physiology 2015, 308: f839-f847. PMID: 25651568, PMCID: PMC4398834, DOI: 10.1152/ajprenal.00601.2014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBicarbonatesBiological TransportCalciumCalcium-Transporting ATPasesChelating AgentsCytosolEnzyme InhibitorsIn Vitro TechniquesInositol 1,4,5-Trisphosphate ReceptorsKidney Tubules, ProximalKineticsMice, Inbred C57BLPerfusionRenal ReabsorptionSodiumSodium-Hydrogen Exchanger 3Sodium-Hydrogen ExchangersConceptsNa/H exchanger 3Luminal Ca(2Flow-induced increaseCytosolic calciumProximal tubulesCa(2+) chelator BAPTA-AMAntagonist 2-aminoethoxydiphenyl borateCa-ATPase inhibitor thapsigarginProximal tubule transportNa(+) reabsorptionMicroperfused in vitroMouse proximal tubuleChelator BAPTA-AMH-ATPase activityNO effectControl tubulesInhibitor thapsigarginBAPTA-AMIntracellular Ca(2Decreased transportTubule transportBaseline transportStimulates Na(+Modulate Na(+Glomerulotubular balance
1999
Induction of Nitric Oxide Synthase mRNA by Shear Stress Requires Intracellular Calcium and G-protein Signals and Is Modulated by PI 3 Kinase
Malek A, Jiang L, Lee I, Sessa W, Izumo S, Alper S. Induction of Nitric Oxide Synthase mRNA by Shear Stress Requires Intracellular Calcium and G-protein Signals and Is Modulated by PI 3 Kinase. Biochemical And Biophysical Research Communications 1999, 254: 231-242. PMID: 9920763, DOI: 10.1006/bbrc.1998.9921.Peer-Reviewed Original ResearchConceptsNitric oxide synthase mRNAPTX-sensitive G proteinsENOS mRNA levelsENOS mRNABovine aortic endothelial cellsIntracellular calciumPertussis toxinMRNA upregulationEndothelial nitric oxide synthase (eNOS) mRNAMRNA levelsEndothelin-1 mRNACalmodulin inhibitor WENOS gene promoterG proteinsSynthase mRNAAortic endothelial cellsTime-dependent increaseTyrosine kinase inhibitor herbimycin ACalcium entryBAPTA-AMInhibitor WEndothelial cellsTyrosine kinase activityMicrotubule integrityLaminar fluid shear stress
1998
Heterologous Expression of the Kv3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons
Whim M, Kaczmarek L. Heterologous Expression of the Kv3.1 Potassium Channel Eliminates Spike Broadening and the Induction of a Depolarizing Afterpotential in the Peptidergic Bag Cell Neurons. Journal Of Neuroscience 1998, 18: 9171-9180. PMID: 9801357, PMCID: PMC6792887, DOI: 10.1523/jneurosci.18-22-09171.1998.Peer-Reviewed Original ResearchConceptsBag cell neuronsCell neuronsAction potentialsCalcium entryUse-dependent inactivationExpression of Kv3.1Kv3.1 potassium channelPeptidergic bag cell neuronsControl neuronsSpontaneous firingBrief synaptic stimulationCalcium currentNeuronal excitabilityIntracellular calciumCalcium influxSynaptic stimulationDepolarizing afterpotentialsBAPTA-AMAfterpotentialsNeuronsPotassium channelsClusters of cellsKv3.1InductionPhysiological role
1996
Ca2+ influx and activation of a cation current are coupled to intracellular Ca2+ release in peptidergic neurons of Aplysia californica.
Knox RJ, Jonas EA, Kao LS, Smith PJ, Connor JA, Kaczmarek LK. Ca2+ influx and activation of a cation current are coupled to intracellular Ca2+ release in peptidergic neurons of Aplysia californica. The Journal Of Physiology 1996, 494: 627-639. PMID: 8865062, PMCID: PMC1160665, DOI: 10.1113/jphysiol.1996.sp021520.Peer-Reviewed Original ResearchConceptsBag cell neuronsCell neuronsThapsigargin-sensitive Ca2Cation currentReversal potentialVoltage-activated Ba2Non-selective cation currentAplysia californicaApparent reversal potentialSteady-state Ca2Thapsigargin-induced elevationMin. 3Endoplasmic reticulum Ca2Voltage-clamp experimentsMicroM tetrodotoxinPeptidergic neuronsIntact gangliaAbdominal ganglionExtracellular Ca2Intracellular Ca2Intracellular storesBAPTA-AMSmall depolarizationBasal levelsNeurons
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