2015
ABT‐737 Inhibits Full Length And Cleaved Pro‐Apoptotic Bcl‐xL, Resulting in Differential Effects on Death And Survival
Park H, Licznerski P, Niu Y, Alavian K, Jonas E. ABT‐737 Inhibits Full Length And Cleaved Pro‐Apoptotic Bcl‐xL, Resulting in Differential Effects on Death And Survival. The FASEB Journal 2015, 29 DOI: 10.1096/fasebj.29.1_supplement.777.4.Peer-Reviewed Original ResearchFull-length Bcl-xLBcl-xLABT-737Mitochondrial potentialATP productionΔN-BclAnti-apoptotic Bcl-2 family proteinsBcl-2 family proteinsCell death stimuliMitochondrial membrane permeabilityATP synthase activityMitochondrial permeability transition porePro-apoptotic BclPro-apoptotic formBcl-xL inhibitorsPermeability transition poreDeath stimuliFamily proteinsBcl-xL.Isolated mitochondriaPharmacological inhibitorsTransition poreCell deathFull lengthSynthase activity
2013
Contributions of Bcl-xL to acute and long term changes in bioenergetics during neuronal plasticity
Jonas EA. Contributions of Bcl-xL to acute and long term changes in bioenergetics during neuronal plasticity. Biochimica Et Biophysica Acta 2013, 1842: 1168-1178. PMID: 24240091, PMCID: PMC4018426, DOI: 10.1016/j.bbadis.2013.11.007.Peer-Reviewed Original ResearchConceptsBcl-xLCaspase activationAnti-death proteinCell death stimuliMitochondrial membrane permeabilitySub-cellular membranesSynaptic vesicle recyclingNeuronal plasticityNormal neuronal plasticityInhibitor ABT-737Ion channel activityMitochondrial Bcl-xLMitochondrial positioningDeath stimuliMitochondrial releaseVesicle recyclingSynaptic growthMitochondrial functionNeurite retractionNeuronal activitySynaptic strengthSynaptic efficacyABT-737Channel activityLong-term decline
2006
Mitochondrial factors with dual roles in death and survival
Cheng WC, Berman SB, Ivanovska I, Jonas EA, Lee SJ, Chen Y, Kaczmarek LK, Pineda F, Hardwick JM. Mitochondrial factors with dual roles in death and survival. Oncogene 2006, 25: 4697-4705. PMID: 16892083, DOI: 10.1038/sj.onc.1209596.Peer-Reviewed Original ResearchConceptsBcl-2 family proteinsCell deathCell death regulatorsPro-death Bcl-2 family proteinNormal cellular functionMitochondrial fission proteinDeath regulatorsDeath stimuliCellular functionsFamily proteinsMitochondrial factorsFission proteinsCell survivalBiochemical mechanismsCaspasesDual roleProteinHealthy cellsCellsMammalsMitochondriaRegulatorSurvivalDeathStretch
2004
Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminals
Jonas EA, Hickman JA, Chachar M, Polster BM, Brandt TA, Fannjiang Y, Ivanovska I, Basañez G, Kinnally KW, Zimmerberg J, Hardwick JM, Kaczmarek LK. Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminals. Proceedings Of The National Academy Of Sciences Of The United States Of America 2004, 101: 13590-13595. PMID: 15342906, PMCID: PMC518799, DOI: 10.1073/pnas.0401372101.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsApoptosisBcl-X ProteinDecapodiformesElectric ConductivityEndopeptidasesHypoxiaIon ChannelsLiposomesMitochondriaNADPatch-Clamp TechniquesPorinsPresynaptic TerminalsProtein Processing, Post-TranslationalProto-Oncogene Proteins c-bcl-2Sequence DeletionVoltage-Dependent Anion ChannelsConceptsBcl-xLMitochondrial channelsDeath pathwaysMitochondrial membraneBcl-xL.Proapoptotic Bcl-2 family proteinsVoltage-dependent anion channelBcl-2 family proteinsOuter mitochondrial membraneCell death pathwaysHydrophobic C-terminusBcl-xL proteinAntiapoptotic Bcl-xLNeuronal death pathwaysDeath stimuliBH3 domainFamily proteinsSquid presynaptic terminalsMammalian cellsC-terminusAnion channelMitochondriaChannel activityOpposite effectHealthy neurons