Elizabeth Jonas, MD
Research & Publications
Biography
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Research Summary
Some of the features of neuronal synaptic transmission that can be modified over the short and long term include changes in presynaptic calcium levels, changes in vesicle numbers and probability of release, and alterations in postsynaptic receptor numbers and function. Such variations account in part for the synaptic plasticity that may underlie learning and memory. Alterations in levels of activity at the synapse require energy and other mitochondrial activities, and therefore mitochondria influence synaptic events by changes in mitochondrial targeting, shape, size and metabolic efficiency. Bcl-2 family proteins, by their actions at mitochondrial membranes, normally play an important role in cell death at the soma, but also strengthen or weaken synaptic connections. Mitochondria also regulate key metabolic events including protein and lipid synthesis required for synaptic plasticity.
Thus the actions of mitochondria at synaptic sites position these organelles to influence physiological and pathological changes in the brain. In neurodegenerative diseases, proteins that control mitochondrial ion channel activity may be key in deciding whether a synapse will live or die, and thereby whether a neuron will survive or undergo untimely death. In neurodevelopmental disease, mitochondrial metabolic changes are required for critical periods in brain and synaptic development.
Specialized Terms: Brain ischemia; Neurodegeneration; Neurodevelopment; Parkinson's Disease; Fragile X Disorder; Autism; Mitochondrial ion channels; Cell death; synaptic transmission; synaptic plasticity; ATP synthase; mitochondrial permeability transition pore (mPTP).
Extensive Research Description
- Role of ATP synthase in prevention of cardiac and brain ischemia: Mitochondrial ATP synthase has been shown recently to be vital not only for cellular energy production but also for energy dissipation and cell death. We identified and characterized a large non-selective uncoupling channel within the ATP synthase c-subunit ring, the persistent opening of which initiates cell death. We have growing evidence for its crucial role in mitochondrial permeability transition (mPT), the opening of a cell death channel that regulates neuronal death during ischemia and neurodegeneration. We have found that the c-ring channel is also required for certain critical periods in brain development, and that normal closing of the channel is required for normal brain and synaptic development. We have now purified ATP synthase from porcine heart mitochondria and performed single-channel studies.
- Structural studies of the ATP synthase c-ring pore: Excised proteoliposome patch-clamp recordings demonstrate that highly pure and fully assembled ATP synthase monomers form large conductance, Ca2+-sensitive and voltage-gated channels. We have confirmed the monomeric state of ATP synthase by cryo-electron microscopy studies of ATP synthase reconstituted into proteoliposomes. We have also heterologously overexpressed and purified human ATP synthase c-subunit fromHEK-293 cells and from E. coli plasma membranes. C-subunit ring purified using this technique forms large conductance channels. C-ring channel is gated by polar amino acid residues situated at the mouth of the pore and by the hydrophilic F1 portion of ATP synthase. We observe dissociation of ATP synthase F1 from FO when we expose primary neurons to glutamate toxicity, suggesting that the non-reversible dissociation of F1 from FO occurs in pathology. We have successfully knocked out five/six alleles of the three genes encoding ATP synthase c-subunit in mouse embryonic stem cells by CRISPR-Cas9, which resulted in 10 percent of the total c-subunit expression. Patch-clamp recordings of mitoplasts isolated from these cells demonstrate low conductance activity that is poorly calcium responsive. These findings confirm that the largest of all inner mitochondrial membrane conductances, and one that forms an uncoupling, non-selective leak channel, resides within the ATP synthase monomer, more specifically within its membrane-embedded c-subunit ring. We are now creating a mouse with a mutant c-subunit that contains a reduced conductance c-subunit. We hypothesize that this mouse will be protected from ischemic heart and brain disease and from degenerative diseases.
- Role of mitochondria in Fragile X disorder: Loss of function of the gene (Fmr1) encoding Fragile X mental retardation protein (FMRP) results in unregulated, elevated mRNA translation and aberrant synaptic morphology. We find that mitochondria in neurons of the Fmr1-/y mouse have an inner membrane leak that undermines ATP synthesis and contributes to a replicative phenotype that is a hallmark of immature, dividing cells. We now find that abnormal stoichiometry leading to increased free ATP synthase c-subunit ring contributes to aberrant mRNA translation in Fmr1-/y mouse neurons and human Fragile X Syndrome (FXS) fibroblasts. C-subunit leak inhibition alters metabolism in favor of oxidative phosphorylation, ushering in a new synaptic developmental period, and this critical change fails to occur in Fragile X synapses. The developmental metabolic switch is also dependent on stimulus-induced phosphorylation of translation elongation factor EF2, an event which is lacking in Fmr1-/y synapses and which changes the mRNAs that are translated. We find that FMRP regulates a stimulus-dependent change in mitochondrial metabolism required for synaptic development.
- Role of Bcl-xL in synaptic plasticity: Long-term potentiation (LTP) and depression (LTD) are the mechanisms that neurons use to modulate their inherent synaptic plasticity and support the storage and recovery of memories in the mammalian brain. The ability to potentiate a synapse over the long term declines significantly in neurodegenerative disorders. In addition to deficiencies in synaptic plasticity, degenerating neurons display acute and chronic mitochondrial dysfunction, suggesting that dysregulated mitochondria play a role in synaptic dysfunction, in addition to their known role in apoptotic cell death. Our previous work has shown that the anti-apoptotic protein Bcl-xL not only prevents somatic cell death, but also potentiates long-term synaptic responses. Here, we show that Bcl-xL is responsible for dramatic changes in ATP levels in hippocampal neurons during LTP. Using fluorescence imaging of a FRET based ATP construct (ATeam) in living hippocampal neurons, we find that LTP induction causes a sharp decrease in ATP levels followed by a persistent long term increase in ATP production. This suggests that after intense synaptic stimulation, neurons may become metabolically more efficient. The long-term increase in ATP levels of LTP-stimulated synapses is blocked by inhibition of Bcl-xL and by inhibition of ATP synthase activity. Bcl-xL inhibition also prevents the long-term increase in surface glutamate receptor insertion. In hippocampal slice recordings, inhibition of Bcl-xL impairs early stage LTP and prevents late stage LTP. Our findings suggest that long term changes in mitochondrial efficiency brought on by activity-dependent translocation of Bcl-xL to mitochondria are required for LTP and shed light upon the role of mitochondrial metabolic programming and dynamics in acute induction and long-term maintenance of learning and memory processing. If such mitochondria-dependent metabolic changes fail to occur, synaptic dysfunction and neurodegeneration may ensue.
- Role of mitochondrial bioenergetics in Parkinson's Disease: Familial Parkinson’s disease (PD) protein DJ-1 mutations are linked to early onset PD. We have found that DJ-1 binds directly to the F1FO ATP synthase β subunit to increase the enzymatic activity of the ATP synthase and enhance the efficiency of ATP production. Mutations in DJ-1 or DJ-1 knock out cause loss of mitochondrial inner membrane coupling, resulting in decreased growth of mouse dopaminergic neuronal processes and human fibroblasts. the reason for this is loss of DJ-1 decreases ATP synthase β subunit levels. DJ-1 improves ATP synthase β subunit levels by boosting its translation and by chaperoning β subunit into the mitochondria. We suggest that DJ-1 maximizes inner membrane efficiency by improving F1/FO ratio. This decreases the inner mitochondrial membrane leak, enhancing dopaminergic neuronal process extension.
Coauthors
Research Interests
Endocrinology; Mitochondria; Nervous System; Synaptic Transmission; Neurobiology; Apoptosis
Research Images
Selected Publications
- Cooperativity of gating of ATP synthase and ant ion channelsJonas E, Shang F, Shen L, Mnatsakanyan N. Cooperativity of gating of ATP synthase and ant ion channels Biophysical Journal 2023, 122: 93a. DOI: 10.1016/j.bpj.2022.11.701.
- Fluid shear stress enhances proliferation of breast cancer cells via downregulation of the c-subunit of the F1FO ATP synthasePark HA, Brown SR, Jansen J, Dunn T, Scott M, Mnatsakanyan N, Jonas EA, Kim Y. Fluid shear stress enhances proliferation of breast cancer cells via downregulation of the c-subunit of the F1FO ATP synthase Biochemical And Biophysical Research Communications 2022, 632: 173-180. PMID: 36209586, PMCID: PMC10024463, DOI: 10.1016/j.bbrc.2022.09.084.
- Mitochondrial ATP synthase F1 subcomplex forms a gate of c-subunit leak channelMnatsakanyan N, Park H, Wu J, Jonas E. Mitochondrial ATP synthase F1 subcomplex forms a gate of c-subunit leak channel Biochimica Et Biophysica Acta (BBA) - Bioenergetics 2022, 1863: 148774. DOI: 10.1016/j.bbabio.2022.148774.
- The Role of Alpha-Tocotrienol during Development of Primary Hippocampal NeuronsPark H, Crowe-White K, Ciesla L, Bannerman S, Scott M, Davis A, Adhikari B, Burnett G, Broman K, Ferdous K, Lackey K, Lickznerski P, Jonas E. The Role of Alpha-Tocotrienol during Development of Primary Hippocampal Neurons Current Developments In Nutrition 2022, 6: 800. PMCID: PMC9194400, DOI: 10.1093/cdn/nzac064.019.
- Mitochondrial ATP synthase c-subunit leak channel triggers cell death upon loss of its F1 subcomplexMnatsakanyan 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.
- Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xLPark HA, Crowe-White KM, Ciesla L, Scott M, Bannerman S, Davis AU, Adhikari B, Burnett G, Broman K, Ferdous KA, Lackey KH, Licznerski P, Jonas EA. Alpha-tocotrienol enhances arborization of primary hippocampal neurons via upregulation of Bcl-xL Progress In Food & Nutrition Science 2022, 101: 31-42. PMID: 35366596, PMCID: PMC9081260, DOI: 10.1016/j.nutres.2022.02.007.
- Alteration of the F1Fo ATP Synthase Causes Metabolic Remodeling in Breast Cancer CellsDunn T, Mnatsakanyan N, Brown S, Jansen J, Hayden M, Jonas E, Kim Y, Park H. Alteration of the F1Fo ATP Synthase Causes Metabolic Remodeling in Breast Cancer Cells Current Developments In Nutrition 2021, 5: 266. PMCID: PMC8182114, DOI: 10.1093/cdn/nzab036_008.
- Vitamin E Improves Neurite Complexity by Enhancing Mitochondrial FunctionPark H, Crowe-White K, Davis A, Bannerman S, Burnett G, Scott M, Broman K, Lackey K, Licznerski P, Jonas E. Vitamin E Improves Neurite Complexity by Enhancing Mitochondrial Function Current Developments In Nutrition 2021, 5: 5140915. PMCID: PMC8181647, DOI: 10.1093/cdn/nzab049_028.
- Wetting Transitions in the ATP Synthase C-Subunit Ring, a Large-Conductance Ion ChannelDotson R, Mnatsakanyan N, Jonas E, Pias S. Wetting Transitions in the ATP Synthase C-Subunit Ring, a Large-Conductance Ion Channel Biophysical Journal 2021, 120: 194a. DOI: 10.1016/j.bpj.2020.11.1335.
- Presynaptic Kv3 channels are required for fast and slow endocytosis of synaptic vesiclesWu XS, Subramanian S, Zhang Y, Shi B, Xia J, Li T, Guo X, El-Hassar L, Szigeti-Buck K, Henao-Mejia J, Flavell RA, Horvath TL, Jonas EA, Kaczmarek LK, Wu LG. Presynaptic Kv3 channels are required for fast and slow endocytosis of synaptic vesicles Neuron 2021, 109: 938-946.e5. PMID: 33508244, PMCID: PMC7979485, DOI: 10.1016/j.neuron.2021.01.006.
- Mitochondria: powerhouses of presynaptic plasticitySubramanian S, Jonas EA. Mitochondria: powerhouses of presynaptic plasticity The Journal Of Physiology 2021, 599: 1363-1364. PMID: 33428213, PMCID: PMC7942974, DOI: 10.1113/jp281040.
- ATP Synthase c-Subunit Leak Causes Aberrant Cellular Metabolism in Fragile X SyndromeLicznerski P, Park HA, Rolyan H, Chen R, Mnatsakanyan N, Miranda P, Graham M, Wu J, Cruz-Reyes N, Mehta N, Sohail S, Salcedo J, Song E, Effman C, Effman S, Brandao L, Xu GN, Braker A, Gribkoff VK, Levy RJ, Jonas EA. ATP Synthase c-Subunit Leak Causes Aberrant Cellular Metabolism in Fragile X Syndrome Cell 2020, 182: 1170-1185.e9. PMID: 32795412, PMCID: PMC7484101, DOI: 10.1016/j.cell.2020.07.008.
- Oxidative stress battles neuronal Bcl-xL in a fight to the deathPark HA, Broman K, Jonas EA. Oxidative stress battles neuronal Bcl-xL in a fight to the death Neural Regeneration Research 2020, 16: 12-15. PMID: 32788441, PMCID: PMC7818872, DOI: 10.4103/1673-5374.286946.
- The new role of F1Fo ATP synthase in mitochondria-mediated neurodegeneration and neuroprotectionMnatsakanyan N, Jonas EA. The new role of F1Fo ATP synthase in mitochondria-mediated neurodegeneration and neuroprotection Experimental Neurology 2020, 332: 113400. PMID: 32653453, PMCID: PMC7877222, DOI: 10.1016/j.expneurol.2020.113400.
- Roles of Vitamin E in Energy Metabolism During Neurite OutgrowthStratton Z, Davis A, Jonas E, Crowe-White K, Park H. Roles of Vitamin E in Energy Metabolism During Neurite Outgrowth Current Developments In Nutrition 2020, 4: nzaa057_051. PMCID: PMC7259054, DOI: 10.1093/cdn/nzaa057_051.
- Cellular Mechanisms of Metabolic Remodeling During Fluid Sheer Stress-Induced MetastasisDunn T, Brown S, Mnatsakanyan N, Jonas E, Yonghyun K, Park H. Cellular Mechanisms of Metabolic Remodeling During Fluid Sheer Stress-Induced Metastasis Current Developments In Nutrition 2020, 4: nzaa044_021. PMCID: PMC7258028, DOI: 10.1093/cdn/nzaa044_021.
- ATP synthase c-subunit ring as the channel of mitochondrial permeability transition: Regulator of metabolism in development and degenerationMnatsakanyan N, Jonas EA. ATP synthase c-subunit ring as the channel of mitochondrial permeability transition: Regulator of metabolism in development and degeneration Journal Of Molecular And Cellular Cardiology 2020, 144: 109-118. PMID: 32461058, PMCID: PMC7877492, DOI: 10.1016/j.yjmcc.2020.05.013.
- Inefficient thermogenic mitochondrial respiration due to futile proton leak in a mouse model of fragile X syndromeGriffiths KK, Wang A, Wang L, Tracey M, Kleiner G, Quinzii CM, Sun L, Yang G, Perez‐Zoghbi J, Licznerski P, Yang M, Jonas EA, Levy RJ. Inefficient thermogenic mitochondrial respiration due to futile proton leak in a mouse model of fragile X syndrome The FASEB Journal 2020, 34: 7404-7426. PMID: 32307754, PMCID: PMC7692004, DOI: 10.1096/fj.202000283rr.
- Structural and Pharmacological Characterization of the Mitochondrial Permeability Transition Pore: A Megachannel Formed by F1FO ATP SynthaseMnatsakanyan N, Llaguno M, Yang Y, Yan Y, Weber J, Sigworth F, Jonas E. Structural and Pharmacological Characterization of the Mitochondrial Permeability Transition Pore: A Megachannel Formed by F1FO ATP Synthase Biophysical Journal 2020, 118: 1a. DOI: 10.1016/j.bpj.2019.11.198.
- Mitochondrial (ATP Synthase) Permeability Transition PoreJonas E, Mnatsakanyan N, Alavian K, Chen R. Mitochondrial (ATP Synthase) Permeability Transition Pore Biophysical Journal 2020, 118: 16a. DOI: 10.1016/j.bpj.2019.11.269.
- Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal NeuronsPark HA, Mnatsakanyan N, Broman K, Davis AU, May J, Licznerski P, Crowe-White KM, Lackey KH, Jonas EA. Alpha-Tocotrienol Prevents Oxidative Stress-Mediated Post-Translational Cleavage of Bcl-xL in Primary Hippocampal Neurons International Journal Of Molecular Sciences 2019, 21: 220. PMID: 31905614, PMCID: PMC6982044, DOI: 10.3390/ijms21010220.
- A mitochondrial megachannel resides in monomeric F1FO ATP synthaseMnatsakanyan N, Llaguno MC, Yang Y, Yan Y, Weber J, Sigworth FJ, Jonas EA. A mitochondrial megachannel resides in monomeric F1FO ATP synthase Nature Communications 2019, 10: 5823. PMID: 31862883, PMCID: PMC6925261, DOI: 10.1038/s41467-019-13766-2.
- Dopamine fuels its own releaseChen R, Jonas EA. Dopamine fuels its own release Nature Neuroscience 2019, 23: 1-2. PMID: 31844312, DOI: 10.1038/s41593-019-0563-4.
- P4‐512: EXCITOTOXIC NEURONAL DEATH INDUCING MEGACHANNEL RESIDES IN MONOMERIC F1FO ATP SYNTHASEMnatsakanyan N, Llaguno M, Yang Y, Yan Y, Sigworth F, Jonas E. P4‐512: EXCITOTOXIC NEURONAL DEATH INDUCING MEGACHANNEL RESIDES IN MONOMERIC F1FO ATP SYNTHASE Alzheimer's & Dementia 2019, 15: p1509-p1510. DOI: 10.1016/j.jalz.2019.08.058.
- Parkinson’s disease protein DJ-1 regulates ATP synthase protein components to increase neuronal process outgrowthChen R, Park HA, Mnatsakanyan N, Niu Y, Licznerski P, Wu J, Miranda P, Graham M, Tang J, Boon AJW, Cossu G, Mandemakers W, Bonifati V, Smith PJS, Alavian KN, Jonas EA. Parkinson’s disease protein DJ-1 regulates ATP synthase protein components to increase neuronal process outgrowth Cell Death & Disease 2019, 10: 469. PMID: 31197129, PMCID: PMC6565618, DOI: 10.1038/s41419-019-1679-x.
- Vitamin E Prevents ΔN-Bcl-xL-associate Mitochondrial Dysfunction in Primary Hippocampal Neurons (P14-024-19).Park HA, Mnatsakanyan N, Broman K, Jonas E. Vitamin E Prevents ΔN-Bcl-xL-associate Mitochondrial Dysfunction in Primary Hippocampal Neurons (P14-024-19). Current Developments In Nutrition 2019, 3 PMID: 31224188, PMCID: PMC6574370, DOI: 10.1093/cdn/nzz052.P14-024-19.
- Vitamin E Prevents ΔN-Bcl-xL-associate Mitochondrial Dysfunction in Primary Hippocampal Neurons (P14-024-19)Park H, Mnatsakanyan N, Broman K, Jonas E. Vitamin E Prevents ΔN-Bcl-xL-associate Mitochondrial Dysfunction in Primary Hippocampal Neurons (P14-024-19) Current Developments In Nutrition 2019, 3: nzz052.p14-024-19. PMCID: PMC6574370, DOI: 10.1093/cdn/nzz052.p14-024-19.
- The mitochondrial metabolic function of DJ‐1 is modulated by 14‐3‐3βWeinert M, Millet A, Jonas EA, Alavian KN. The mitochondrial metabolic function of DJ‐1 is modulated by 14‐3‐3β The FASEB Journal 2019, 33: 8925-8934. PMID: 31034784, PMCID: PMC6988861, DOI: 10.1096/fj.201802754r.
- Activation of Slack Potassium Channels (KCNT1) Triggers an Increase in mRNA TranslationMalone T, Licznerski P, Jonas E, Kaczmarek L. Activation of Slack Potassium Channels (KCNT1) Triggers an Increase in mRNA Translation Biophysical Journal 2019, 116: 306a. DOI: 10.1016/j.bpj.2018.11.1658.
- Mitochondrial Megachannel Resides in Monomeric ATP SynthaseMnatsakanyan N, Park H, Jing W, Llaguno M, Murtishi B, Latta M, Davis E, Miranda P, Yang Y, Sigworth F, Jonas E. Mitochondrial Megachannel Resides in Monomeric ATP Synthase Biophysical Journal 2019, 116: 156a. DOI: 10.1016/j.bpj.2018.11.863.
- ATP Synthase C-Subunit-Deficient Mitochondria Have a Small Cyclosporine A-Sensitive Channel, but Lack the Permeability Transition PoreNeginskaya MA, Solesio ME, Berezhnaya EV, Amodeo GF, Mnatsakanyan N, Jonas EA, Pavlov EV. ATP Synthase C-Subunit-Deficient Mitochondria Have a Small Cyclosporine A-Sensitive Channel, but Lack the Permeability Transition Pore Cell Reports 2019, 26: 11-17.e2. PMID: 30605668, PMCID: PMC6521848, DOI: 10.1016/j.celrep.2018.12.033.
- Nutritional Regulators of Bcl-xL in the BrainPark HA, Broman K, Stumpf A, Kazyak S, Jonas EA. Nutritional Regulators of Bcl-xL in the Brain Molecules 2018, 23: 3019. PMID: 30463183, PMCID: PMC6278276, DOI: 10.3390/molecules23113019.
- ATP synthase in neuronal development, neurodegeneration and plasticityJonas E, Licznerski P, Chen R, Rolyan H, Gribkoff V, Mnatsakanyan N. ATP synthase in neuronal development, neurodegeneration and plasticity Biochimica Et Biophysica Acta (BBA) - Bioenergetics 2018, 1859: e30. DOI: 10.1016/j.bbabio.2018.09.095.
- The role of ATP synthase megachannel in mitochondrial permeability transitionMnatsakanyan N, Park H, Wu J, Miranda P, Jonas E. The role of ATP synthase megachannel in mitochondrial permeability transition Biochimica Et Biophysica Acta (BBA) - Bioenergetics 2018, 1859: e112. DOI: 10.1016/j.bbabio.2018.09.330.
- Cardiac metabolic effects of KNa1.2 channel deletion and evidence for its mitochondrial localizationSmith CO, Wang YT, Nadtochiy SM, Miller JH, Jonas EA, Dirksen RT, Nehrke K, Brookes PS. Cardiac metabolic effects of KNa1.2 channel deletion and evidence for its mitochondrial localization The FASEB Journal 2018, 32: 6135-6149. PMID: 29863912, PMCID: PMC6181635, DOI: 10.1096/fj.201800139r.
- BDNF signaling: Harnessing stress to battle mood disorderLicznerski P, Jonas EA. BDNF signaling: Harnessing stress to battle mood disorder Proceedings Of The National Academy Of Sciences Of The United States Of America 2018, 115: 3742-3744. PMID: 29592951, PMCID: PMC5899500, DOI: 10.1073/pnas.1803645115.
- Molecular Composition, Structure and Regulation of the Mitochondrial Permeability Transition PoreMnatsakanyan N, Park H, Wu J, Miranda P, Jonas E. Molecular Composition, Structure and Regulation of the Mitochondrial Permeability Transition Pore Biophysical Journal 2018, 114: 658a. DOI: 10.1016/j.bpj.2017.11.3555.
- Molecular Assembly of the Mitochondrial Permeability Transition PoreAmodeo G, Mnatsakanyan N, Solesio M, Klim M, Kurcok P, Zakharian E, Jonas E, Pavlov E. Molecular Assembly of the Mitochondrial Permeability Transition Pore Biophysical Journal 2018, 114: 658a. DOI: 10.1016/j.bpj.2017.11.3554.
- Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseasesConnolly NMC, Theurey P, Adam-Vizi V, Bazan NG, Bernardi P, Bolaños JP, Culmsee C, Dawson VL, Deshmukh M, Duchen MR, Düssmann H, Fiskum G, Galindo MF, Hardingham GE, Hardwick JM, Jekabsons MB, Jonas EA, Jordán J, Lipton SA, Manfredi G, Mattson MP, McLaughlin B, Methner A, Murphy AN, Murphy MP, Nicholls DG, Polster BM, Pozzan T, Rizzuto R, Satrústegui J, Slack RS, Swanson RA, Swerdlow RH, Will Y, Ying Z, Joselin A, Gioran A, Moreira Pinho C, Watters O, Salvucci M, Llorente-Folch I, Park DS, Bano D, Ankarcrona M, Pizzo P, Prehn JHM. Guidelines on experimental methods to assess mitochondrial dysfunction in cellular models of neurodegenerative diseases Cell Death & Differentiation 2017, 25: 542-572. PMID: 29229998, PMCID: PMC5864235, DOI: 10.1038/s41418-017-0020-4.
- Phylogenetic Profiling of Mitochondrial Proteins and Integration Analysis of Bacterial Transcription Units Suggest Evolution of F1Fo ATP Synthase from Multiple ModulesNiu Y, Moghimyfiroozabad S, Safaie S, Yang Y, Jonas EA, Alavian KN. Phylogenetic Profiling of Mitochondrial Proteins and Integration Analysis of Bacterial Transcription Units Suggest Evolution of F1Fo ATP Synthase from Multiple Modules Journal Of Molecular Evolution 2017, 85: 219-233. PMID: 29177973, PMCID: PMC5709465, DOI: 10.1007/s00239-017-9819-3.
- Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicityPark HA, Licznerski P, Mnatsakanyan N, Niu Y, Sacchetti S, Wu J, Polster BM, Alavian KN, Jonas EA. Inhibition of Bcl-xL prevents pro-death actions of ΔN-Bcl-xL at the mitochondrial inner membrane during glutamate excitotoxicity Cell Death & Differentiation 2017, 24: 1963-1974. PMID: 28777375, PMCID: PMC5635221, DOI: 10.1038/cdd.2017.123.
- The Mitochondrial Permeability Transition Pore: Molecular Structure and Function in Health and DiseaseJonas E, Porter G, Beutner G, Mnatsakanyan N, Park H, Mehta N, Chen R, Alavian K. The Mitochondrial Permeability Transition Pore: Molecular Structure and Function in Health and Disease 2017, 69-105. DOI: 10.1007/978-3-319-55539-3_3.
- Examination of Mitochondrial Ion Conductance by Patch Clamp in Intact Neurons and Mitochondrial Membrane PreparationsJonas E, Mnatsakanyan N. Examination of Mitochondrial Ion Conductance by Patch Clamp in Intact Neurons and Mitochondrial Membrane Preparations 2017, 123: 211-238. DOI: 10.1007/978-1-4939-6890-9_11.
- Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and NecroptosisZille M, Karuppagounder SS, Chen Y, Gough PJ, Bertin J, Finger J, Milner TA, Jonas EA, Ratan RR. Neuronal Death After Hemorrhagic Stroke In Vitro and In Vivo Shares Features of Ferroptosis and Necroptosis Stroke 2017, 48: 1033-1043. PMID: 28250197, PMCID: PMC5613764, DOI: 10.1161/strokeaha.116.015609.
- Mitochondria and Memory: Bioenergetics, Synaptic Plasticity and NeurodegenerationJonas E, Mnatsakanyan N, Miranda P, Park H, Chen R, Licznerski P, Weinert M, Smith P, Chavez A, Zukin R, Gribkoff V, Alavian K. Mitochondria and Memory: Bioenergetics, Synaptic Plasticity and Neurodegeneration Biophysical Journal 2017, 112: 180a. DOI: 10.1016/j.bpj.2016.11.996.
- New Insights into the Molecular Structure and Regulation of the Mitochondrial Permeability Transition PoreMnatsakanyan N, Park H, Wu J, Miranda P, Jonas E. New Insights into the Molecular Structure and Regulation of the Mitochondrial Permeability Transition Pore Biophysical Journal 2017, 112: 440a. DOI: 10.1016/j.bpj.2016.11.2349.
- ΔN-Bcl-xL, a therapeutic target for neuroprotectionPark HA, Jonas EA. ΔN-Bcl-xL, a therapeutic target for neuroprotection Neural Regeneration Research 2017, 12: 1791-1794. PMID: 29239317, PMCID: PMC5745825, DOI: 10.4103/1673-5374.219033.
- Erratum to: The Mitochondrial Permeability Transition Pore and ATP SynthaseBeutner G, Alavian KN, Jonas EA, Porter GA. Erratum to: The Mitochondrial Permeability Transition Pore and ATP Synthase 2016, 240: 489-489. PMID: 27913888, DOI: 10.1007/164_2016_87.
- The MIFstep in parthanatosJonas E. The MIFstep in parthanatos Science 2016, 354: 36-37. PMID: 27846484, DOI: 10.1126/science.aai8756.
- Editorial notePeixoto PM, Pavlov E, Jonas E. Editorial note Journal Of Bioenergetics And Biomembranes 2016, 49: 1-2. PMID: 27714488, DOI: 10.1007/s10863-016-9679-3.
- The Mitochondrial Permeability Transition Pore and ATP SynthaseBeutner G, Alavian K, Jonas EA, Porter GA. The Mitochondrial Permeability Transition Pore and ATP Synthase 2016, 240: 21-46. PMID: 27590224, PMCID: PMC7439278, DOI: 10.1007/164_2016_5.
- PTP and LTP: The physiological role of the permeability transition pore in learning and memoryJonas E, Miranda P, Gribkoff V, Alavian K, Park H, Wu J, Chavez A, Zukin R, Hardwick J, Mnatsakanyan N. PTP and LTP: The physiological role of the permeability transition pore in learning and memory Biochimica Et Biophysica Acta (BBA) - Bioenergetics 2016, 1857: e66-e67. DOI: 10.1016/j.bbabio.2016.04.357.
- The role of ATP synthase in mitochondrial permeability transition, neuronal death and survivalMnatsakanyan N, Park H, Wu J, Miranda P, Jonas E. The role of ATP synthase in mitochondrial permeability transition, neuronal death and survival Biochimica Et Biophysica Acta (BBA) - Bioenergetics 2016, 1857: e68. DOI: 10.1016/j.bbabio.2016.04.362.
- Physiological roles of the mitochondrial permeability transition poreMnatsakanyan N, Beutner G, Porter GA, Alavian KN, Jonas EA. Physiological roles of the mitochondrial permeability transition pore Journal Of Bioenergetics And Biomembranes 2016, 49: 13-25. PMID: 26868013, PMCID: PMC4981558, DOI: 10.1007/s10863-016-9652-1.
- Mitochondrial Permeability Transition Pore (mPTP) Formation Requires the Participation of c-Subunit of ATP-Synthase, Polyhydroxybutyrate (PHB) and Inorganic Polyphosphate (polyP)Elustondo P, Mnatsakanyan N, Eleonora Z, Jonas E, Pavlov E. Mitochondrial Permeability Transition Pore (mPTP) Formation Requires the Participation of c-Subunit of ATP-Synthase, Polyhydroxybutyrate (PHB) and Inorganic Polyphosphate (polyP) Biophysical Journal 2016, 110: 310a. DOI: 10.1016/j.bpj.2015.11.1666.
- A Novel Ion Channel in ATP Synthase C-Subunit Ring: Gatekeeper of Life and DeathMnatsakanyan N, Park H, Wu J, Miranda P, Jonas E. A Novel Ion Channel in ATP Synthase C-Subunit Ring: Gatekeeper of Life and Death Biophysical Journal 2016, 110: 310a. DOI: 10.1016/j.bpj.2015.11.1664.
- Decreased SGK1 Expression and Function Contributes to Behavioral Deficits Induced by Traumatic StressLicznerski P, Duric V, Banasr M, Alavian KN, Ota KT, Kang HJ, Jonas EA, Ursano R, Krystal JH, Duman RS, . Decreased SGK1 Expression and Function Contributes to Behavioral Deficits Induced by Traumatic Stress PLOS Biology 2015, 13: e1002282. PMID: 26506154, PMCID: PMC4623974, DOI: 10.1371/journal.pbio.1002282.
- The Mitochondrial Permeability Transition Pore, the c‐Subunit of the F1Fo ATP Synthase, Cellular Development, and Synaptic EfficiencyJonas E, Porter G, Beutner G, Mnatsakanyan N, Alavian K. The Mitochondrial Permeability Transition Pore, the c‐Subunit of the F1Fo ATP Synthase, Cellular Development, and Synaptic Efficiency 2015, 31-64. DOI: 10.1002/9781119017127.ch2.
- Cell death disguised: The mitochondrial permeability transition pore as the c-subunit of the F1FO ATP synthaseJonas EA, Porter GA, Beutner G, Mnatsakanyan N, Alavian KN. Cell death disguised: The mitochondrial permeability transition pore as the c-subunit of the F1FO ATP synthase Pharmacological Research 2015, 99: 382-392. PMID: 25956324, PMCID: PMC4567435, DOI: 10.1016/j.phrs.2015.04.013.
- ABT‐737 Inhibits Full Length And Cleaved Pro‐Apoptotic Bcl‐xL, Resulting in Differential Effects on Death And SurvivalPark 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.
- Bcl-xL Is Necessary for Neurite Outgrowth in Hippocampal NeuronsPark HA, Licznerski P, Alavian KN, Shanabrough M, Jonas EA. Bcl-xL Is Necessary for Neurite Outgrowth in Hippocampal Neurons Antioxidants And Redox Signaling 2015, 22: 93-108. PMID: 24787232, PMCID: PMC4281845, DOI: 10.1089/ars.2013.5570.
- The Mitochondrial Complex V–Associated Large-Conductance Inner Membrane Current Is Regulated by Cyclosporine and DexpramipexoleAlavian KN, Dworetzky SI, Bonanni L, Zhang P, Sacchetti S, Li H, Signore AP, Smith PJ, Gribkoff VK, Jonas EA. The Mitochondrial Complex V–Associated Large-Conductance Inner Membrane Current Is Regulated by Cyclosporine and Dexpramipexole Molecular Pharmacology 2014, 87: 1-8. PMID: 25332381, PMCID: PMC4279080, DOI: 10.1124/mol.114.095661.
- Bcl-xL in neuroprotection and plasticityJonas 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.
- Abstract 110: Anesthetic Preconditioning and Mitochondrial Slo K + Channel Activity Require Slo2.1Wojtovich A, Smith C, Nadtochiy S, Urciuoli W, Xia X, Jonas E, Lingle C, Nehrke K, Brookes P. Abstract 110: Anesthetic Preconditioning and Mitochondrial Slo K + Channel Activity Require Slo2.1 Circulation Research 2014, 115 DOI: 10.1161/res.115.suppl_1.110.
- An uncoupling channel within the c-subunit ring of the F1FO ATP synthase is the mitochondrial permeability transition poreAlavian KN, Beutner G, Lazrove E, Sacchetti S, Park HA, Licznerski P, Li H, Nabili P, Hockensmith K, Graham M, Porter GA, Jonas EA. An uncoupling channel within the c-subunit ring of the F1FO ATP synthase is the mitochondrial permeability transition pore Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 10580-10585. PMID: 24979777, PMCID: PMC4115574, DOI: 10.1073/pnas.1401591111.
- Impaired import: how huntingtin harmsJonas EA. Impaired import: how huntingtin harms Nature Neuroscience 2014, 17: 747-749. PMID: 24866036, PMCID: PMC4448962, DOI: 10.1038/nn.3726.
- Fluorescent Measurement of Synaptic Activity Using SynaptopHluorin in Isolated Hippocampal Neurons.Li H, Park HA, Jonas EA. Fluorescent Measurement of Synaptic Activity Using SynaptopHluorin in Isolated Hippocampal Neurons. Bio-protocol 2014, 4 PMID: 27446978, PMCID: PMC4950945, DOI: 10.21769/bioprotoc.1304.
- Mitochondrial membrane protein Bcl-xL, a regulator of adult neuronal growth and synaptic plasticity: multiple functions beyond apoptosisPark HA, Jonas EA. Mitochondrial membrane protein Bcl-xL, a regulator of adult neuronal growth and synaptic plasticity: multiple functions beyond apoptosis Neural Regeneration Research 2014, 9: 1706-1707. PMID: 25422630, PMCID: PMC4238157, DOI: 10.4103/1673-5374.143413.
- The C-Subunit of the ATP Synthase Forms the Pore of the PTPJonas E, Sacchetti S, Park H, Lazrove E, Beutner G, Porter G, Alavian K. The C-Subunit of the ATP Synthase Forms the Pore of the PTP Biophysical Journal 2014, 106: 3a-4a. DOI: 10.1016/j.bpj.2013.11.049.
- Contributions of Bcl-xL to acute and long term changes in bioenergetics during neuronal plasticityJonas 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.
- A Bcl-xL–Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosisLi H, Alavian KN, Lazrove E, Mehta N, Jones A, Zhang P, Licznerski P, Graham M, Uo T, Guo J, Rahner C, Duman RS, Morrison RS, Jonas EA. A Bcl-xL–Drp1 complex regulates synaptic vesicle membrane dynamics during endocytosis Nature Cell Biology 2013, 15: 773-785. PMID: 23792689, PMCID: PMC3725990, DOI: 10.1038/ncb2791.
- F1FO ATPase vesicle preparation and technique for performing patch clamp recordings of submitochondrial vesicle membranes.Sacchetti S, Alavian KN, Lazrove E, Jonas EA. F1FO ATPase vesicle preparation and technique for performing patch clamp recordings of submitochondrial vesicle membranes. Journal Of Visualized Experiments 2013, e4394. PMID: 23685483, PMCID: PMC3676267, DOI: 10.3791/4394.
- F1FO ATPase Vesicle Preparation and Technique for Performing Patch Clamp Recordings of Submitochondrial Vesicle MembranesSacchetti S, Alavian K, Lazrove E, Jonas E. F1FO ATPase Vesicle Preparation and Technique for Performing Patch Clamp Recordings of Submitochondrial Vesicle Membranes Journal Of Visualized Experiments 2013 DOI: 10.3791/4394-v.
- PINK1 protects against cell death induced by mitochondrial depolarization, by phosphorylating Bcl-xL and impairing its pro-apoptotic cleavageArena G, Gelmetti V, Torosantucci L, Vignone D, Lamorte G, De Rosa P, Cilia E, Jonas EA, Valente EM. PINK1 protects against cell death induced by mitochondrial depolarization, by phosphorylating Bcl-xL and impairing its pro-apoptotic cleavage Cell Death & Differentiation 2013, 20: 920-930. PMID: 23519076, PMCID: PMC3679455, DOI: 10.1038/cdd.2013.19.
- DJ1 regulates Neuronal Mitochondrial Bioenergetic EfficiencyJonas E, Lazrove E, Nabili P, Alavian K. DJ1 regulates Neuronal Mitochondrial Bioenergetic Efficiency Biophysical Journal 2013, 104: 657a. DOI: 10.1016/j.bpj.2012.11.3628.
- Multipolar functions of BCL-2 proteins link energetics to apoptosisHardwick JM, Chen YB, Jonas EA. Multipolar functions of BCL-2 proteins link energetics to apoptosis Trends In Cell Biology 2012, 22: 318-328. PMID: 22560661, PMCID: PMC3499971, DOI: 10.1016/j.tcb.2012.03.005.
- NAD kinase regulates the size of the NADPH pool and insulin secretion in pancreatic β-cellsGray JP, Alavian KN, Jonas EA, Heart EA. NAD kinase regulates the size of the NADPH pool and insulin secretion in pancreatic β-cells AJP Endocrinology And Metabolism 2012, 303: e191-e199. PMID: 22550069, PMCID: PMC3431206, DOI: 10.1152/ajpendo.00465.2011.
- N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal deathOfengeim D, Chen YB, Miyawaki T, Li H, Sacchetti S, Flannery RJ, Alavian KN, Pontarelli F, Roelofs BA, Hickman JA, Hardwick JM, Zukin RS, Jonas EA. N-terminally cleaved Bcl-xL mediates ischemia-induced neuronal death Nature Neuroscience 2012, 15: 574-580. PMID: 22366758, PMCID: PMC3862259, DOI: 10.1038/nn.3054.
- Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiencyAlavian KN, Dworetzky SI, Bonanni L, Zhang P, Sacchetti S, Mariggio MA, Onofrj M, Thomas A, Li H, Mangold JE, Signore AP, DeMarco U, Demady DR, Nabili P, Lazrove E, Smith PJ, Gribkoff VK, Jonas EA. Effects of dexpramipexole on brain mitochondrial conductances and cellular bioenergetic efficiency Brain Research 2012, 1446: 1-11. PMID: 22364637, PMCID: PMC3746080, DOI: 10.1016/j.brainres.2012.01.046.
- Mouse Transient Global Ischemia Two-Vessel Occlusion Model.Pontarelli F, Ofengeim D, Zukin RS, Jonas EA. Mouse Transient Global Ischemia Two-Vessel Occlusion Model. Bio-protocol 2012, 2 PMID: 27446974, PMCID: PMC4950949, DOI: 10.21769/bioprotoc.262.
- The C-Subunit Ring of the F1FO ATP Synthase Constitutes a Leak Channel that Regulates Cellular Metabolic Efficiency by Counteracting the H+ TranslocatorAlavian K, Lazrove E, Nabili P, Li H, Jonas E. The C-Subunit Ring of the F1FO ATP Synthase Constitutes a Leak Channel that Regulates Cellular Metabolic Efficiency by Counteracting the H+ Translocator Biophysical Journal 2012, 102: 571a. DOI: 10.1016/j.bpj.2011.11.3110.
- Erratum: Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthaseAlavian K, Li H, Collis L, Bonanni L, Zeng L, Sacchetti S, Lazrove E, Nabili P, Flaherty B, Graham M, Chen Y, Messerli S, Mariggio M, Rahner C, McNay E, Shore G, Smith P, Hardwick J, Jonas E. Erratum: Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase Nature Cell Biology 2011, 13: 1383-1383. DOI: 10.1038/ncb2369.
- Bcl-x L regulates mitochondrial energetics by stabilizing the inner membrane potentialChen Y, Aon M, Hsu Y, Soane L, Teng X, McCaffery J, Cheng W, Qi B, Li H, Alavian K, Dayhoff-Brannigan M, Zou S, Pineda F, O'Rourke B, Ko Y, Pedersen P, Kaczmarek L, Jonas E, Hardwick J. Bcl-x L regulates mitochondrial energetics by stabilizing the inner membrane potential Journal Of Experimental Medicine 2011, 208: i29-i29. DOI: 10.1084/jem20811oia29.
- Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potentialChen YB, Aon MA, Hsu YT, Soane L, Teng X, McCaffery JM, Cheng WC, Qi B, Li H, Alavian KN, Dayhoff-Brannigan M, Zou S, Pineda FJ, O'Rourke B, Ko YH, Pedersen PL, Kaczmarek LK, Jonas EA, Hardwick JM. Bcl-xL regulates mitochondrial energetics by stabilizing the inner membrane potential Journal Of Cell Biology 2011, 195: 263-276. PMID: 21987637, PMCID: PMC3198165, DOI: 10.1083/jcb.201108059.
- Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthaseAlavian KN, Li H, Collis L, Bonanni L, Zeng L, Sacchetti S, Lazrove E, Nabili P, Flaherty B, Graham M, Chen Y, Messerli SM, Mariggio MA, Rahner C, McNay E, Shore GC, Smith PJ, Hardwick JM, Jonas EA. Bcl-xL regulates metabolic efficiency of neurons through interaction with the mitochondrial F1FO ATP synthase Nature Cell Biology 2011, 13: 1224-1233. PMID: 21926988, PMCID: PMC3186867, DOI: 10.1038/ncb2330.
- Hoofbeats and zebras: neurodegenerative disorder presenting as a “first episode” of psychosisOzkan B, Phutane V, Jonas E, Tek C, Srihari V. Hoofbeats and zebras: neurodegenerative disorder presenting as a “first episode” of psychosis General Hospital Psychiatry 2011, 33: 412.e1-412.e3. PMID: 21762843, PMCID: PMC3139144, DOI: 10.1016/j.genhosppsych.2011.03.011.
- Decrease in a Leak Conductance Associated with Mitochondrial Complex V and Improved Bioenergetic Efficiency may Underlie Cytoprotection of at-Risk Neurons by DexpramipexoleSacchetti S, Dworetzky S, Alavian K, Zhang P, Bonanni L, Signore A, Mangold J, DeMarco U, Smith P, Gribkoff V, Jonas E. Decrease in a Leak Conductance Associated with Mitochondrial Complex V and Improved Bioenergetic Efficiency may Underlie Cytoprotection of at-Risk Neurons by Dexpramipexole Biophysical Journal 2011, 100: 459a. DOI: 10.1016/j.bpj.2010.12.2701.
- Bcl-xL Determines the Metabolic Efficiency of Neurons, through Interaction with Mitochondrial ATP SynthaseAlavian K, Li H, Sacchetti S, Nabili P, Lazrove E, Bonanni L, Smith P, Hardwick J, Jonas E. Bcl-xL Determines the Metabolic Efficiency of Neurons, through Interaction with Mitochondrial ATP Synthase Biophysical Journal 2011, 100: 459a. DOI: 10.1016/j.bpj.2010.12.2700.
- BCL-xL Regulates ATP Synthase and Synaptic EfficiencyAlavian K, Collis L, Li H, Zeng L, Bonanni L, Rahner C, Hardwick J, Jonas E. BCL-xL Regulates ATP Synthase and Synaptic Efficiency Biophysical Journal 2010, 98: 465a. DOI: 10.1016/j.bpj.2009.12.2527.
- Molecular participants in mitochondrial cell death channel formation during neuronal ischemiaJonas EA. Molecular participants in mitochondrial cell death channel formation during neuronal ischemia Experimental Neurology 2009, 218: 203-212. PMID: 19341732, PMCID: PMC2710418, DOI: 10.1016/j.expneurol.2009.03.025.
- Bcl-xL increases mitochondrial fission, fusion, and biomass in neuronsBerman 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.
- Bcl-xl Regulates ATP Synthase Activity at the Inner Mitochondrial MembraneJonas E, Collis L, Li H, Zeng L, Bonanni L, Pypaert M, McNay E, Cline G, Smith P, Hardwick J. Bcl-xl Regulates ATP Synthase Activity at the Inner Mitochondrial Membrane Biophysical Journal 2009, 96: 538a. DOI: 10.1016/j.bpj.2008.12.2775.
- Mitochondrial Ion Channels in Ischemic BrainJonas E. Mitochondrial Ion Channels in Ischemic Brain 2009, 117-150. DOI: 10.1007/978-1-60327-579-8_7.
- Unique Mitochondrial Ion Channels: Roles in Synaptic Transmission and Programmed Cell DeathJonas E. Unique Mitochondrial Ion Channels: Roles in Synaptic Transmission and Programmed Cell Death 2008, 155-191. DOI: 10.1002/9780470429907.ch6.
- Ischemic preconditioning blocks BAD translocation, Bcl-xL cleavage, and large channel activity in mitochondria of postischemic hippocampal neuronsMiyawaki T, Mashiko T, Ofengeim D, Flannery RJ, Noh KM, Fujisawa S, Bonanni L, Bennett MV, Zukin RS, Jonas EA. Ischemic preconditioning blocks BAD translocation, Bcl-xL cleavage, and large channel activity in mitochondria of postischemic hippocampal neurons Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 4892-4897. PMID: 18347331, PMCID: PMC2290755, DOI: 10.1073/pnas.0800628105.
- PKC-Induced Intracellular Trafficking of CaV2 Precedes Its Rapid Recruitment to the Plasma MembraneZhang Y, Helm JS, Senatore A, Spafford JD, Kaczmarek LK, Jonas EA. PKC-Induced Intracellular Trafficking of CaV2 Precedes Its Rapid Recruitment to the Plasma Membrane Journal Of Neuroscience 2008, 28: 2601-2612. PMID: 18322103, PMCID: PMC2830008, DOI: 10.1523/jneurosci.4314-07.
- Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neuronsLi H, Chen Y, Jones AF, Sanger RH, Collis LP, Flannery R, McNay EC, Yu T, Schwarzenbacher R, Bossy B, Bossy-Wetzel E, Bennett MV, Pypaert M, Hickman JA, Smith PJ, Hardwick JM, Jonas EA. Bcl-xL induces Drp1-dependent synapse formation in cultured hippocampal neurons Proceedings Of The National Academy Of Sciences Of The United States Of America 2008, 105: 2169-2174. PMID: 18250306, PMCID: PMC2542873, DOI: 10.1073/pnas.0711647105.
- Bcl-xL Inhibitor ABT-737 Reveals a Dual Role for Bcl-xL in Synaptic TransmissionHickman 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.
- Expression of the Voltage-Gated Sodium Channel NaV1.5 in the Macrophage Late Endosome Regulates Endosomal AcidificationCarrithers MD, Dib-Hajj S, Carrithers LM, Tokmoulina G, Pypaert M, Jonas EA, Waxman SG. Expression of the Voltage-Gated Sodium Channel NaV1.5 in the Macrophage Late Endosome Regulates Endosomal Acidification The Journal Of Immunology 2007, 178: 7822-7832. PMID: 17548620, DOI: 10.4049/jimmunol.178.12.7822.
- Hypoxia increases BK channel activity in the inner mitochondrial membraneGu XQ, Siemen D, Parvez S, Cheng Y, Xue J, Zhou D, Sun X, Jonas EA, Haddad GG. Hypoxia increases BK channel activity in the inner mitochondrial membrane Biochemical And Biophysical Research Communications 2007, 358: 311-316. PMID: 17481584, DOI: 10.1016/j.bbrc.2007.04.110.
- Mitochondrial factors with dual roles in death and survivalCheng 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.
- 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.
- Zinc-Dependent Multi-Conductance Channel Activity in Mitochondria Isolated from Ischemic BrainBonanni L, Chachar M, Jover-Mengual T, Li H, Jones A, Yokota H, Ofengeim D, Flannery RJ, Miyawaki T, Cho CH, Polster BM, Pypaert M, Hardwick JM, Sensi SL, Zukin RS, Jonas EA. Zinc-Dependent Multi-Conductance Channel Activity in Mitochondria Isolated from Ischemic Brain Journal Of Neuroscience 2006, 26: 6851-6862. PMID: 16793892, PMCID: PMC4758341, DOI: 10.1523/jneurosci.5444-05.2006.
- Regulation of Synaptic Stability by Bcl‐2 Family ProteinsKaczmarek L, Jonas E. Regulation of Synaptic Stability by Bcl‐2 Family Proteins CNS Neuroscience & Therapeutics 2006, 6: 30-31. DOI: 10.1111/j.1527-3458.2000.tb00175.x.
- Actions of BAX on Mitochondrial Channel Activity and on Synaptic TransmissionJonas EA, Hardwick JM, Kaczmarek LK. Actions of BAX on Mitochondrial Channel Activity and on Synaptic Transmission Antioxidants And Redox Signaling 2005, 7: 1092-1100. PMID: 16115013, DOI: 10.1089/ars.2005.7.1092.
- The Role of the Mitochondrial Apoptosis Induced Channel MAC in Cytochrome c ReleaseMartinez-Caballero S, Dejean LM, Jonas EA, Kinnally KW. The Role of the Mitochondrial Apoptosis Induced Channel MAC in Cytochrome c Release Journal Of Bioenergetics And Biomembranes 2005, 37: 155-164. PMID: 16167172, DOI: 10.1007/s10863-005-6570-z.
- Oligomeric Bax Is a Component of the Putative Cytochrome c Release Channel MAC, Mitochondrial Apoptosis-induced ChannelDejean LM, Martinez-Caballero S, Guo L, Hughes C, Teijido O, Ducret T, Ichas F, Korsmeyer SJ, Antonsson B, Jonas EA, Kinnally KW. Oligomeric Bax Is a Component of the Putative Cytochrome c Release Channel MAC, Mitochondrial Apoptosis-induced Channel Molecular Biology Of The Cell 2005, 16: 2424-2432. PMID: 15772159, PMCID: PMC1087246, DOI: 10.1091/mbc.e04-12-1111.
- Exposure to Hypoxia Rapidly Induces Mitochondrial Channel Activity within a Living Synapse*Jonas EA, Hickman JA, Hardwick JM, Kaczmarek LK. Exposure to Hypoxia Rapidly Induces Mitochondrial Channel Activity within a Living Synapse* Journal Of Biological Chemistry 2004, 280: 4491-4497. PMID: 15561723, DOI: 10.1074/jbc.m410661200.
- Proapoptotic N-truncated BCL-xL protein activates endogenous mitochondrial channels in living synaptic terminalsJonas 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.
- Regulation of Synaptic Transmission by Mitochondrial Ion ChannelsJonas E. Regulation of Synaptic Transmission by Mitochondrial Ion Channels Journal Of Bioenergetics And Biomembranes 2004, 36: 357-361. PMID: 15377872, DOI: 10.1023/b:jobb.0000041768.11006.90.
- Ion channels on intracellular organellesKaczmarek L, Jonas E. Ion channels on intracellular organelles 2004, 32: 433-458. DOI: 10.1016/s1569-2558(03)32018-1.
- Modulation of Synaptic Transmission by the BCL-2 Family Protein BCL-xLJonas EA, Hoit D, Hickman JA, Brandt TA, Polster BM, Fannjiang Y, McCarthy E, Montanez MK, Hardwick JM, Kaczmarek LK. Modulation of Synaptic Transmission by the BCL-2 Family Protein BCL-xL Journal Of Neuroscience 2003, 23: 8423-8431. PMID: 12968005, PMCID: PMC6740692, DOI: 10.1523/jneurosci.23-23-08423.2003.
- Modulation of mitochondrial function by endogenous Zn2+ poolsSensi SL, Ton-That D, Sullivan PG, Jonas EA, Gee KR, Kaczmarek LK, Weiss JH. Modulation of mitochondrial function by endogenous Zn2+ pools Proceedings Of The National Academy Of Sciences Of The United States Of America 2003, 100: 6157-6162. PMID: 12724524, PMCID: PMC156342, DOI: 10.1073/pnas.1031598100.
- BAK Alters Neuronal Excitability and Can Switch from Anti- to Pro-Death Function during Postnatal DevelopmentFannjiang 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.
- Prolonged Activation of Mitochondrial Conductances During Synaptic TransmissionJonas E, Buchanan J, Kaczmarek L. Prolonged Activation of Mitochondrial Conductances During Synaptic Transmission Science 1999, 286: 1347-1350. PMID: 10558987, DOI: 10.1126/science.286.5443.1347.
- Giga-Ohm Seals on Intracellular Membranes: A Technique for Studying Intracellular Ion Channels in Intact CellsJonas E, Knox R, Kaczmarek L. Giga-Ohm Seals on Intracellular Membranes: A Technique for Studying Intracellular Ion Channels in Intact Cells Neuron 1997, 19: 7-13. PMID: 9247259, DOI: 10.1016/s0896-6273(00)80343-8.
- Regulation by insulin of a unique neuronal Ca2+ pool and of neuropeptide secretionJonas E, Knox R, Smith T, Wayne N, Connor J, Kaczmarek L. Regulation by insulin of a unique neuronal Ca2+ pool and of neuropeptide secretion Nature 1997, 385: 343-346. PMID: 9002519, DOI: 10.1038/385343a0.
- 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.
- Regulation of potassium channels by protein kinasesJonas E, Kaczmarek L. Regulation of potassium channels by protein kinases Current Opinion In Neurobiology 1996, 6: 318-323. PMID: 8794088, DOI: 10.1016/s0959-4388(96)80114-0.
- Insulin receptor in Aplysia neurons: characterization, molecular cloning, and modulation of ion currentsJonas E, Knox R, Kaczmarek L, Schwartz J, Solomon D. Insulin receptor in Aplysia neurons: characterization, molecular cloning, and modulation of ion currents Journal Of Neuroscience 1996, 16: 1645-1658. PMID: 8774433, PMCID: PMC6578688, DOI: 10.1523/jneurosci.16-05-01645.1996.