Mitochondrial Small Conductance SK2 Channels Prevent Glutamate-induced Oxytosis and Mitochondrial Dysfunction (606 views)
Jbc Papers (ISSN: 0021-9258, 1083-351x, 0021-9258linking), 2013 Apr 12; 288(15): 10792-10804.
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Paper type: Journal Article, Research Support, Non-U. S. Gov'T,
Impact factor: 4.6, 5-year impact factor: 4.863
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84876209070&partnerID=40&md5=909782a7be2b3dbe4740b43e999b6cd5
Keywords: Animals, Cell Line, Cell Membrane Genetics Metabolism Pathology, Glutamic Acid Genetics Metabolism Pharmacology, Membrane Potential, Mitochondrial Drug Effects Genetics, Mitochondria Genetics Metabolism Pathology, Mitochondrial Membranes Metabolism Pathology, Nerve Tissue Proteins Genetics Metabolism, Neurons Metabolism Pathology, Neuroprotective Agents Pharmacology, Peptides Pharmacology, Potassium Metabolism, Small-Conductance Calcium-Activated Potassium Channels Antagonists, Inhibitors Genetics Metabolism, Inhibitory Peptides, Inner Mitochondrial Membranes, Intermembrane Space, Mitochondrial Dysfunction, Mitochondrial Protein, Mitochondrial Transmembrane Potentials, Patch Clamp Recording, Bioelectric Potentials, Cell Death, Electrophysiology, N Methyl Dextro Aspartic Acid Receptor, Proapoptotic Mitochondrial Protein, Sk2 Channel, Small Conductance Calcium Activated Potassium Channel, Small Interfering Rna, Unclassified Drug, Amino Terminal Sequence, Animal Cell, Carboxy Terminal Sequence, Controlled Study, Disorders Of Mitochondrial Functions, Mouse, Nonhuman, Potassium Current, Priority Journal, Protein Function, Protein Localization, Protein Rna Binding, Protein Secretion, Protein Targeting,
Affiliations:
*** IBB - CNR ***
Institut fur Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universitat Marburg, D-35032 Marburg, Germany. dolga@staff.uni-marburg.de
Institut für Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universität Marburg, D-35032 Marburg, Germany
Institut für Physiologie und Pathophysiologie, Vegetative Physiologie, Fachbereich Medizin, D-35037 Marburg, Germany
Department of Systems Biology and Medicine, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02114, United States
Gene Center, Ludwig Maximilians University, Feodor-Lynen Strasse 25, 81377 Munich, Germany
Department of Neurodegeneration, Royal College of Surgeons in Ireland, Dublin 2, Ireland
Institute of Biostructures and Bioimaging, National Research Council (CNR), 16-80131 Naples, Italy
Institute of Stroke and Dementia Research, University of Munich Medical School, D-81377 Munich, Germany
Institute of Toxicology, Helmholtz Zentrum München-German Research Center for Environmental Health (GmbH), D-85764 Neuherberg, Germany
Institut f r Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universit t Marburg, D-35032 Marburg, Germany
Institut f r Physiologie und Pathophysiologie, Vegetative Physiologie, Fachbereich Medizin, D-35037 Marburg, Germany
References:
Not available.
Jbc Papers (ISSN: 0021-9258, 1083-351x, 0021-9258linking), 2013 Apr 12; 288(15): 10792-10804.
Export to BibTeX Export to EndNote
Paper type: Journal Article, Research Support, Non-U. S. Gov'T,
Impact factor: 4.6, 5-year impact factor: 4.863
Url: http://www.scopus.com/inward/record.url?eid=2-s2.0-84876209070&partnerID=40&md5=909782a7be2b3dbe4740b43e999b6cd5
Keywords: Animals, Cell Line, Cell Membrane Genetics Metabolism Pathology, Glutamic Acid Genetics Metabolism Pharmacology, Membrane Potential, Mitochondrial Drug Effects Genetics, Mitochondria Genetics Metabolism Pathology, Mitochondrial Membranes Metabolism Pathology, Nerve Tissue Proteins Genetics Metabolism, Neurons Metabolism Pathology, Neuroprotective Agents Pharmacology, Peptides Pharmacology, Potassium Metabolism, Small-Conductance Calcium-Activated Potassium Channels Antagonists, Inhibitors Genetics Metabolism, Inhibitory Peptides, Inner Mitochondrial Membranes, Intermembrane Space, Mitochondrial Dysfunction, Mitochondrial Protein, Mitochondrial Transmembrane Potentials, Patch Clamp Recording, Bioelectric Potentials, Cell Death, Electrophysiology, N Methyl Dextro Aspartic Acid Receptor, Proapoptotic Mitochondrial Protein, Sk2 Channel, Small Conductance Calcium Activated Potassium Channel, Small Interfering Rna, Unclassified Drug, Amino Terminal Sequence, Animal Cell, Carboxy Terminal Sequence, Controlled Study, Disorders Of Mitochondrial Functions, Mouse, Nonhuman, Potassium Current, Priority Journal, Protein Function, Protein Localization, Protein Rna Binding, Protein Secretion, Protein Targeting,
Affiliations:
*** IBB - CNR ***
Institut fur Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universitat Marburg, D-35032 Marburg, Germany. dolga@staff.uni-marburg.de
Institut für Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universität Marburg, D-35032 Marburg, Germany
Institut für Physiologie und Pathophysiologie, Vegetative Physiologie, Fachbereich Medizin, D-35037 Marburg, Germany
Department of Systems Biology and Medicine, Harvard Medical School and Massachusetts General Hospital, Boston, MA 02114, United States
Gene Center, Ludwig Maximilians University, Feodor-Lynen Strasse 25, 81377 Munich, Germany
Department of Neurodegeneration, Royal College of Surgeons in Ireland, Dublin 2, Ireland
Institute of Biostructures and Bioimaging, National Research Council (CNR), 16-80131 Naples, Italy
Institute of Stroke and Dementia Research, University of Munich Medical School, D-81377 Munich, Germany
Institute of Toxicology, Helmholtz Zentrum München-German Research Center for Environmental Health (GmbH), D-85764 Neuherberg, Germany
Institut f r Pharmakologie und Klinische Pharmazie, Fachbereich Pharmazie, Philipps-Universit t Marburg, D-35032 Marburg, Germany
Institut f r Physiologie und Pathophysiologie, Vegetative Physiologie, Fachbereich Medizin, D-35037 Marburg, Germany
References:
Not available.
Mitochondrial Small Conductance SK2 Channels Prevent Glutamate-induced Oxytosis and Mitochondrial Dysfunction
Small conductance calcium-activated potassium (SK2/K(Ca)2.2) channels are known to be located in the neuronal plasma membrane where they provide feedback control of NMDA receptor activity. Here, we provide evidence that SK2 channels are also located in the inner mitochondrial membrane of neuronal mitochondria. Patch clamp recordings in isolated mitoplasts suggest insertion into the inner mitochondrial membrane with the C and N termini facing the intermembrane space. Activation of SK channels increased mitochondrial K+ currents, whereas channel inhibition attenuated these currents. In a model of glutamate toxicity, activation of SK2 channels attenuated the loss of the mitochondrial transmembrane potential, blocked mitochondrial fission, prevented the release of proapoptotic mitochondrial proteins, and reduced cell death. Neuroprotection was blocked by specific SK2 inhibitory peptides and siRNA targeting SK2 channels. Activation of mitochondrial SK2 channels may therefore represent promising targets for neuroprotective strategies in conditions of mitochondrial dysfunction.
Small conductance calcium-activated potassium (SK2/K(Ca)2.2) channels are known to be located in the neuronal plasma membrane where they provide feedback control of NMDA receptor activity. Here, we provide evidence that SK2 channels are also located in the inner mitochondrial membrane of neuronal mitochondria. Patch clamp recordings in isolated mitoplasts suggest insertion into the inner mitochondrial membrane with the C and N termini facing the intermembrane space. Activation of SK channels increased mitochondrial K+ currents, whereas channel inhibition attenuated these currents. In a model of glutamate toxicity, activation of SK2 channels attenuated the loss of the mitochondrial transmembrane potential, blocked mitochondrial fission, prevented the release of proapoptotic mitochondrial proteins, and reduced cell death. Neuroprotection was blocked by specific SK2 inhibitory peptides and siRNA targeting SK2 channels. Activation of mitochondrial SK2 channels may therefore represent promising targets for neuroprotective strategies in conditions of mitochondrial dysfunction.
Mitochondrial Small Conductance SK2 Channels Prevent Glutamate-induced Oxytosis and Mitochondrial Dysfunction
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Mitochondrial Small Conductance SK2 Channels Prevent Glutamate-induced Oxytosis and Mitochondrial Dysfunction
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* Interaction between AIF and CHCHD4 Regulates Respiratory Chain Biogenesis (662 views)
Mol Cell (ISSN: 1097-2765, 1097-4164), 2015; 58(6): 1001-1014.
Impact Factor: 13.958
View Export to BibTeX Export to EndNote
Oppermann S, Schrader FC, Elsasser K, Dolga AM, Kraus AL, Doti N, Wegscheid-Gerlach C, Schlitzer M, Culmsee C
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View Export to BibTeX Export to EndNote
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Cell Death & (ISSN: 2041-4889, 2041-4889electronic), 2014 Jan 16; 5(1): e993-e993.
Impact Factor: 5.014
View Export to BibTeX Export to EndNote
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J Am Heart Assoc Journal Of The American Heart Association (ISSN: 2047-9980), 2013 May 20; 2(3): e000086-e000086.
Impact Factor: 2.882
View Export to BibTeX Export to EndNote
Zannetti A, Iommelli F, Fonti R, Papaccioli A, Sommella J, Lettieri A, Pirozzi G, Bianco R, Tortora G, Salvatore M, Del Vecchio S
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Impact Factor: 6.488
View Export to BibTeX Export to EndNote
Atlante A, Amadoro G, Bobba A, de Bari L, Corsetti V, Pappalardo G, Marra E, Calissano P, Passarella S
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Bba-Gen Subjects (ISSN: 0005-2728, 0006-3002print, 0006-3002linking), 2008; 1777(10): 1289-1300.
Impact Factor: 4.447
View Export to BibTeX Export to EndNote
Russo M, Palumbo R, Tedesco I, Mazzarella G, Russo P, Iacomino G, Russo GL
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Impact Factor: 3.72
View Export to BibTeX Export to EndNote
7 Records (5 excluding Abstracts).
Total impact factor: 40.481 (32.585 excluding Abstracts).
Total 5 year impact factor: 40.826 (32.653 excluding Abstracts).
Total impact factor: 40.481 (32.585 excluding Abstracts).
Total 5 year impact factor: 40.826 (32.653 excluding Abstracts).
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