2009
Bcl-xL increases mitochondrial fission, fusion, and biomass in neurons
Berman SB, Chen YB, Qi B, McCaffery JM, Rucker EB, Goebbels S, Nave KA, Arnold BA, Jonas EA, Pineda FJ, Hardwick JM. Bcl-xL increases mitochondrial fission, fusion, and biomass in neurons. Journal Of Cell Biology 2009, 184: 707-719. PMID: 19255249, PMCID: PMC2686401, DOI: 10.1083/jcb.200809060.Peer-Reviewed Original ResearchConceptsMitochondrial fissionMitochondrial morphologyCell deathApoptotic cell deathRate of fissionMitochondrial organellesOrganelle morphologyMitochondrial biomassBcl-xLCell typesFluorescence microscopyHealthy neuronsBclCultured neuronsDependent mechanismNeuronal dysfunctionFissionNeuronal processesBiomassSynaptic activityFusionOrganellesComputational strategyRate of fusionRegulation
2007
Bcl-xL Inhibitor ABT-737 Reveals a Dual Role for Bcl-xL in Synaptic Transmission
Hickman JA, Hardwick JM, Kaczmarek LK, Jonas EA. Bcl-xL Inhibitor ABT-737 Reveals a Dual Role for Bcl-xL in Synaptic Transmission. Journal Of Neurophysiology 2007, 99: 1515-1522. PMID: 18160428, PMCID: PMC2836590, DOI: 10.1152/jn.00598.2007.Peer-Reviewed Original ResearchConceptsMitochondrial outer membraneEndogenous Bcl-xLMitochondrial channel activityBcl-xLInhibitor ABT-737ABT-737Outer membraneBcl-xL.Pro-apoptotic cleavage productRecombinant Bcl-xLChannel activityBcl-xL proteinSynaptic functionDual roleGenetic toolsDomain pocketSynaptic transmissionSynaptic activityGiant presynaptic terminalEquivalent modificationEndogenous proteolysisRepetitive synaptic activityBH3Cleavage productsProtein
2006
BCL-xL regulates synaptic plasticity.
Jonas E. BCL-xL regulates synaptic plasticity. Molecular Interventions 2006, 6: 208-22. PMID: 16960143, DOI: 10.1124/mi.6.4.7.Peer-Reviewed Original ResearchConceptsBcl-xLSynaptic vesicle recyclingRole of mitochondriaHigh synaptic activityMembrane ion pumpsMitochondrial localizationCalcium homeostasisVesicle recyclingPresynaptic terminalsPredominant organellesCell deathSynaptic vesiclesSynaptic developmentIon pumpsIntracellular calcium homeostasisRecent discoveryMitochondriaSynaptic transmitter releaseHomeostasisSynaptic plasticitySynaptic sitesSynapseSynaptic processesSynaptic activityOrganelles
2003
BAK Alters Neuronal Excitability and Can Switch from Anti- to Pro-Death Function during Postnatal Development
Fannjiang Y, Kim CH, Huganir RL, Zou S, Lindsten T, Thompson CB, Mito T, Traystman RJ, Larsen T, Griffin DE, Mandir AS, Dawson TM, Dike S, Sappington AL, Kerr DA, Jonas EA, Kaczmarek LK, Hardwick JM. BAK Alters Neuronal Excitability and Can Switch from Anti- to Pro-Death Function during Postnatal Development. Developmental Cell 2003, 4: 575-585. PMID: 12689595, DOI: 10.1016/s1534-5807(03)00091-1.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAnimalsAnimals, NewbornApoptosisBcl-2 Homologous Antagonist-Killer ProteinCentral Nervous SystemCentral Nervous System DiseasesCentral Nervous System Viral DiseasesDisease Models, AnimalEpilepsyExcitatory Postsynaptic PotentialsGenetic VectorsHippocampusKainic AcidMaleMembrane ProteinsMiceMice, KnockoutNeurodegenerative DiseasesNeuronsNeurotoxinsProtein Structure, TertiarySindbis VirusStrokeSynaptic TransmissionConceptsNeuronal excitabilityVirus infectionPostnatal developmentAlters neuronal excitabilityKainate-induced seizuresSpinal cord neuronsIschemia/strokeSindbis virus infectionNeuronal injuryCord neuronsNeuronal deathProtective effectSynaptic activityMouse modelParkinson's diseaseNeuron subtypesNeurotransmitter releasePro-death functionMiceNeuronsSpecific death stimuliDeathSeizuresPossible roleExcitability