CCC1 Suppresses Mitochondrial Damage in the Yeast Model of Friedreich's Ataxia by Limiting Mitochondrial Iron Accumulation
Open Access
- 1 March 2000
- journal article
- Published by Elsevier in Journal of Biological Chemistry
- Vol. 275 (11) , 7626-7632
- https://doi.org/10.1074/jbc.275.11.7626
Abstract
No abstract availableKeywords
This publication has 18 references indexed in Scilit:
- Direct evidence that mitochondrial iron accumulation occurs in Friedreich ataxiaAnnals of Neurology, 1999
- The Friedreich's ataxia mutation confers cellular sensitivity to oxidant stress which is rescued by chelators of iron and calcium and inhibitors of apoptosisHuman Molecular Genetics, 1999
- The Yeast Frataxin Homologue Mediates Mitochondrial Iron EffluxJournal of Biological Chemistry, 1999
- Frataxin is Reduced in Friedreich Ataxia Patients and is Associated with Mitochondrial MembranesHuman Molecular Genetics, 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
- Regulation of Mitochondrial Iron Accumulation by Yfh1p, a Putative Homolog of FrataxinScience, 1997
- The role of the Saccharomyces cerevisiae CCC1 gene in the homeostasis of manganese ionsMolecular Microbiology, 1996
- XII. Yeast sequencing reports. Sequence, mapping and disruption of CCC1, a gene that cross‐complements the Ca2+‐sensitive phenotype of csg1 mutantsYeast, 1994
- The Cardiomyopathy of Friedreich's Ataxia Morphological Observations in 3 CasesCanadian Journal of Neurological Sciences, 1980