Pathogenesis of human mitochondrial diseases is modulated by reduced activity of the ubiquitin/proteasome system

Mitochondria maintain cellular homeostasis by coordinating ATP synthesis with metabolic activity, redox signaling, and apoptosis. Excessive levels of mitochondria-derived reactive oxygen species (ROS) promote mitochondrial dysfunction, triggering numerous metabolic disorders. However, the molecular...

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Bibliographic Details
Published in:	Cell metabolism Vol. 19; no. 4; p. 642
Main Authors:	Segref, Alexandra, Kevei, Éva, Pokrzywa, Wojciech, Schmeisser, Kathrin, Mansfeld, Johannes, Livnat-Levanon, Nurit, Ensenauer, Regina, Glickman, Michael H, Ristow, Michael, Hoppe, Thorsten
Format:	Journal Article
Language:	English
Published:	United States 01.04.2014
Subjects:	Adenosine Triphosphate - metabolism Animals Animals, Genetically Modified Caenorhabditis elegans Cell Line Cyclooxygenase 1 - genetics Electrophoresis, Polyacrylamide Gel Green Fluorescent Proteins Humans Immunoblotting Mitochondrial Diseases - metabolism Mitochondrial Diseases - physiopathology Mutagenesis Organic Chemicals Oxidative Phosphorylation Proteasome Endopeptidase Complex - metabolism Proteolysis Reactive Oxygen Species - metabolism Ubiquitin - metabolism Ubiquitin-Protein Ligases - metabolism
ISSN:	1932-7420, 1932-7420
Online Access:	Get more information
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