2022
Mitochondrial ATP synthase c-subunit leak channel triggers cell death upon loss of its F1 subcomplex
Mnatsakanyan N, Park HA, Wu J, He X, Llaguno MC, Latta M, Miranda P, Murtishi B, Graham M, Weber J, Levy RJ, Pavlov EV, Jonas EA. Mitochondrial ATP synthase c-subunit leak channel triggers cell death upon loss of its F1 subcomplex. Cell Death & Differentiation 2022, 29: 1874-1887. PMID: 35322203, PMCID: PMC9433415, DOI: 10.1038/s41418-022-00972-7.Peer-Reviewed Original ResearchConceptsMitochondrial permeability transitionATP synthase c-subunitCell deathMitochondrial ATP synthaseChannel activityCellular energy productionLeak channelsVoltage-gated ion channelsF1 subcomplexATP synthaseC subunitInner membraneProkaryotic hostsCell stressPermeability transitionIon channelsGating mechanismOsmotic changesLarge conductanceC-ringChannels triggersNeuronal deathF1SubcomplexOsmotic gradient
2014
Bcl-xL in neuroprotection and plasticity
Jonas EA, Porter GA, Alavian KN. Bcl-xL in neuroprotection and plasticity. Frontiers In Physiology 2014, 5: 355. PMID: 25278904, PMCID: PMC4166110, DOI: 10.3389/fphys.2014.00355.BooksMitochondrial outer membrane permeabilizationBcl-xLSynapse formationOuter membrane permeabilizationMaster regulator proteinBcl-2 family member Bcl-xLPro-death factorsPro-apoptotic factorsNeurodegenerative diseasesVesicular traffickingSpecialized proteinsRegulator proteinMembrane permeabilizationCell stressBioenergetic efficiencyHigh metabolic demandsNeurodegenerative stimuliProteinNormal neuronal activityChannel activityNeuronal functionGenetic mutationsSuch protective strategiesNeuroprotective strategiesNeuronal death