Abstract:
:Friedreich ataxia is the most common recessive neurodegenerative disease and is caused by reduced expression of mitochondrial frataxin. Frataxin depletion causes impairment in iron-sulfur cluster and heme biosynthesis, disruption of iron homeostasis and hypersensitivity to oxidants. Currently no pharmacological treatment blocks disease progression, although antioxidant therapies proved to benefit patients. We show that sensitivity of yeast frataxin-deficient cells to hydrogen peroxide is partially mediated by the metacaspase. Metacaspase deletion in frataxin-deficient cells results in recovery of antioxidant capacity and heme synthesis. In addition, our results suggest that metacaspase is associated with mitochondrial respiration, intracellular redox control and genomic stability.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Lefevre S,Sliwa D,Auchère F,Brossas C,Ruckenstuhl C,Boggetto N,Lesuisse E,Madeo F,Camadro JM,Santos Rdoi
10.1016/j.febslet.2011.12.002subject
Has Abstractpub_date
2012-01-20 00:00:00pages
143-8issue
2eissn
0014-5793issn
1873-3468pii
S0014-5793(11)00872-6journal_volume
586pub_type
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