| Literature DB >> 9843204 |
Z Zhu1, J Yao, T Johns, K Fu, I De Bie, C Macmillan, A P Cuthbert, R F Newbold, J Wang, M Chevrette, G K Brown, R M Brown, E A Shoubridge.
Abstract
Leigh Syndrome (LS) is a severe neurological disorder characterized by bilaterally symmetrical necrotic lesions in subcortical brain regions that is commonly associated with systemic cytochrome c oxidase (COX) deficiency. COX deficiency is an autosomal recessive trait and most patients belong to a single genetic complementation group. DNA sequence analysis of the genes encoding the structural subunits of the COX complex has failed to identify a pathogenic mutation. Using microcell-mediated chromosome transfer, we mapped the gene defect in this disorder to chromosome 9q34 by complementation of the respiratory chain deficiency in patient fibroblasts. Analysis of a candidate gene (SURF1) of unknown function revealed several mutations, all of which predict a truncated protein. These data suggest a role for SURF1 in the biogenesis of the COX complex and define a new class of gene defects causing human neurodegenerative disease.Entities:
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Year: 1998 PMID: 9843204 DOI: 10.1038/3804
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330