The MCK mouse heart model of Friedreich's ataxia: Alterations in iron-regulated proteins and cardiac hypertrophy are limited by iron chelation
Author:
Publisher
Proceedings of the National Academy of Sciences
Subject
Multidisciplinary
Reference33 articles.
1. Friedreich's Ataxia: Autosomal Recessive Disease Caused by an Intronic GAA Triplet Repeat Expansion
2. Regulation of Mitochondrial Iron Accumulation by Yfh1p, a Putative Homolog of Frataxin
3. Aconitase and mitochondrial iron–sulphur protein deficiency in Friedreich ataxia
4. Respiratory deficiency due to loss of mitochondrial DNA in yeast lacking the frataxin homologue
5. Mouse models for Friedreich ataxia exhibit cardiomyopathy, sensory nerve defect and Fe-S enzyme deficiency followed by intramitochondrial iron deposits
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