Friedreich’s ataxia is a mitochondrial disorder
- 28 September 1999
- journal article
- editorial
- Published by Proceedings of the National Academy of Sciences in Proceedings of the National Academy of Sciences
- Vol. 96 (20) , 10948-10949
- https://doi.org/10.1073/pnas.96.20.10948
Abstract
No abstract availableThis publication has 21 references indexed in Scilit:
- Deficit of in vivo mitochondrial ATP production in patients with Friedreich ataxiaProceedings of the National Academy of Sciences, 1999
- Direct evidence that mitochondrial iron accumulation occurs in Friedreich ataxia.1999
- Sticky DNAMolecular Cell, 1999
- Aconitase and mitochondrial iron–sulphur protein deficiency in Friedreich ataxiaNature Genetics, 1997
- Frataxin gene of Friedreich's ataxia is targeted to mitochondriaAnnals of Neurology, 1997
- Respiratory deficiency due to loss of mitochondrial DNA in yeast lacking the frataxin homologueNature Genetics, 1997
- Studies of human, mouse and yeast homologues indicate a mitochondrial function for frataxinNature Genetics, 1997
- Phenotype Correlation and Intergenerational Dynamics of the Friedreich Ataxia GAA Trinucleotide RepeatAmerican Journal of Human Genetics, 1997
- Regulation of Mitochondrial Iron Accumulation by Yfh1p, a Putative Homolog of FrataxinScience, 1997
- Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat ExpansionScience, 1996