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MARCH5 inactivation supports mitochondrial function during neurodegenerative stress

Fang, Lei and Li, Jia and Flammer, Josef and Neutzner, Albert. (2013) MARCH5 inactivation supports mitochondrial function during neurodegenerative stress. Frontiers in cellular neuroscience, Vol. 7. p. 176.

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Official URL: http://edoc.unibas.ch/dok/A6338231

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Abstract

Neuronal cell death is accompanied by mitochondrial dysfunction with mitochondrial maintenance critical to neuronal survival. The mitochondrial ubiquitin ligase MARCH5 has dual roles in the upkeep of mitochondrial function. MARCH5 is involved in targeted degradation of proteins harmful to mitochondria and impacts mitochondrial morphology upstream of the fission protein Drp1. In a neuronal cell model, dominant-negative MARCH5 prevents mitochondrial fragmentation during neurodegenerative stress induced by the neuron-specific reactive oxygen generator 6-hydroxydopamine, the complex I inhibitor rotenone or Alzheimer's-related amyloid beta peptide. In addition, preservation of mitochondrial function in terms of membrane potential and lower reactive oxygen generation was observed following inactivation of MARCH5. Our findings connect MARCH5 to neuronal stress responses and further emphasize the link between mitochondrial dynamics and function.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Ocular Pharmacology and Physiology (Neutzner/Meyer)
UniBasel Contributors:Neutzner, Albert
Item Type:Article, refereed
Article Subtype:Research Article
Bibsysno:Link to catalogue
Publisher:Frontiers Research Foundation
Note:Publication type according to Uni Basel Research Database: Journal article
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Last Modified:04 Sep 2015 14:32
Deposited On:10 Apr 2015 09:12

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