Journal
EMBO MOLECULAR MEDICINE
Volume 6, Issue 2, Pages 155-157Publisher
WILEY
DOI: 10.1002/emmm.201303586
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Funding
- Academy of Finland
- University of Helsinki
- Sigrid Juselius Foundation
- U.S. National Institutes of Health [HD32062]
- Department of Defense [W911NF-12-1-0159]
- Muscular Dystrophy Association
- Ellison Medical Foundation
- J. Willard and Alice S. Marriott Foundation
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Mutations in mitochondrial DNA are an important cause of human disease and from a therapeutic standpoint, these disorders are currently untreatable. New studies now show that a non-cognate mitochondrial aminoacyl tRNA synthetase can overcome the respiratory defect caused by an mt-tRNA mutation and that the isolated carboxy-terminal domain of human mt-leucyl tRNA synthetase can ameliorate the pathologic phenotype.
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