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Open Access
Peer-reviewed
Research Article
Loss of UCP2 Attenuates Mitochondrial Dysfunction without Altering ROS Production and Uncoupling Activity
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Alexandra Kukat,
Affiliations Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Institute for Mitochondrial Diseases and Aging, Medical Faculty, University of Cologne, Cologne, Germany, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden
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Sukru Anil Dogan,
Affiliation Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Institute for Mitochondrial Diseases and Aging, Medical Faculty, University of Cologne, Cologne, Germany
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Daniel Edgar,
Affiliation Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden
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Arnaud Mourier,
Affiliation Max Planck Institute for Biology of Aging, Cologne, Germany
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Christoph Jacoby,
Affiliation Department of Cardiovascular Physiology, Heinrich-Heine-University, Düsseldorf, Germany
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Priyanka Maiti,
Affiliation Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Institute for Mitochondrial Diseases and Aging, Medical Faculty, University of Cologne, Cologne, Germany
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Jan Mauer,
Affiliation Max Planck Institute for Neurological Research, Cologne, Germany
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Christina Becker,
Affiliation Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Institute for Mitochondrial Diseases and Aging, Medical Faculty, University of Cologne, Cologne, Germany
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Katharina Senft,
Affiliation Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Institute for Mitochondrial Diseases and Aging, Medical Faculty, University of Cologne, Cologne, Germany
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Rolf Wibom,
Affiliation Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden
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Alexei P. Kudin,
Affiliation Department of Epileptology, University of Bonn, Bonn, Germany
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Kjell Hultenby,
Affiliation Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden
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Ulrich Flögel,
Affiliation Department of Cardiovascular Physiology, Heinrich-Heine-University, Düsseldorf, Germany
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Stephan Rosenkranz,
Affiliations Department III of Internal Medicine, University of Cologne, Cologne, Germany, Cologne Cardiovascular Research Center (CCRC) and Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany
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Daniel Ricquier,
Affiliation University Paris Descartes, Faculty of Medicine, CNRS FRE3210, Paris, France
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Wolfram S. Kunz,
Affiliation Department of Epileptology, University of Bonn, Bonn, Germany
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Aleksandra Trifunovic
* E-mail: aleksandra.trifunovic@uk-koeln.de
Affiliations Cologne Excellence Cluster on Cellular Stress Responses in Aging-Associated Diseases (CECAD) and Institute for Mitochondrial Diseases and Aging, Medical Faculty, University of Cologne, Cologne, Germany, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden, Cologne Cardiovascular Research Center (CCRC) and Center for Molecular Medicine Cologne, University of Cologne, Cologne, Germany
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Loss of UCP2 Attenuates Mitochondrial Dysfunction without Altering ROS Production and Uncoupling Activity
- Alexandra Kukat,
- Sukru Anil Dogan,
- Daniel Edgar,
- Arnaud Mourier,
- Christoph Jacoby,
- Priyanka Maiti,
- Jan Mauer,
- Christina Becker,
- Katharina Senft,
- Rolf Wibom
- Published: June 19, 2014
- https://doi.org/10.1371/journal.pgen.1004385