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Overexpression of Drosophila frataxin triggers cell death in an iron-dependent manner

Edenharter, Oliver, Clement, Janik, Schneuwly, Stephan and Navarro, Juan A. (2017) Overexpression of Drosophila frataxin triggers cell death in an iron-dependent manner. Journal of Neurogenetics 31 (4), pp. 189-202.

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Other URL: http://doi.org/10.1080/01677063.2017.1363200


Friedreich ataxia (FRDA) is the most important autosomal recessive ataxia in the Caucasian population. FRDA patients display severe neurological and cardiac symptoms that reflect a strong cellular and axonal degeneration. FRDA is caused by a loss of function of the mitochondrial protein frataxin which impairs the biosynthesis of iron-sulfur clusters and in turn the catalytic activity of several ...


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Item type:Article
Institutions:Biology, Preclinical Medicine > Institut für Zoologie > Entwicklungsbiologie (Prof. Dr. Stephan Schneuwly)
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Keywords:FRIEDREICHS-ATAXIA; OXIDATIVE STRESS; PARKINSONS-DISEASE; LIFE-SPAN; MITOCHONDRIAL DYSFUNCTION; CLUSTER FORMATION; LIPID-METABOLISM; HDAC INHIBITORS; MODEL; DEFICIENCY; Drosophila melanogaster; frataxin; overexpression; neuronal death; oxidative stress; mitochondrial morphology; iron metabolism; mitoferrin
Dewey Decimal Classification:500 Science > 590 Zoological sciences
Refereed:Yes, this version has been refereed
Created at the University of Regensburg:Yes
Item ID:38827
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