Inactivation of mitochondrial aspartate aminotransferase contributes to the respiratory deficit of yeast frataxin-deficient cells

Biochem. J. (2011) Immediate Publication, doi:10.1042/BJ20111574
Dominika Sliwa, Julien Dairou, Jean-Michel Camadro and Renata Santos
Institut Jacques Monod, Paris, France

Keywords: Friedreich ataxia, frataxin, iron homeostasis, hypersensitivity to oxidants, NAD+ and NADH, malate-aspartate NADH shuttle, mitochondrial aspartate aminotransferase (Aat1), mitochondrial acetylated proteins, post-translational modification.

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