| Literature DB >> 9894887 |
A L Andreu1, C Bruno, T C Dunne, K Tanji, S Shanske, C M Sue, S Krishna, G M Hadjigeorgiou, A Shtilbans, E Bonilla, S DiMauro.
Abstract
We describe a new mitochondrial DNA mutation in the cytochrome b gene in a patient presenting with progressive exercise intolerance and myoglobinuria associated with complex III deficiency in muscle. The point mutation results in the replacement of a glycine at amino acid position 190 with a stop codon. This change predicts premature termination of translation, leading to a truncated protein missing 244 amino acids at the C-terminus of cytochrome b. The mutation fulfills all the accepted criteria for pathogenicity, suggesting that this is the primary cause of the myopathy in the patient.Entities:
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Year: 1999 PMID: 9894887 DOI: 10.1002/1531-8249(199901)45:1<127::aid-art20>3.0.co;2-y
Source DB: PubMed Journal: Ann Neurol ISSN: 0364-5134 Impact factor: 10.422