| Literature DB >> 10522901 |
G Pari1, M M Crerar, J Nalbantoglu, E Shoubridge, A Jani, S Tsujino, S Shanske, S DiMauro, J M Howell, G Karpati.
Abstract
McArdle's disease is due to a genetic deficiency of glycogen phosphorylase and results in a lack of glucose mobilization from glycogen during anaerobic exercise. A genetic defect in Merino sheep produces a similar picture. We constructed a first-generation adenoviral recombinant containing the full-length human phosphorylase cDNA under the control of the Rous sarcoma virus promoter. Primary myoblast cultures from phosphorylase-deficient human and sheep muscle were efficiently transduced with this vector, resulting in restoration of the phosphorylase activity. A similar correction of the genetic defect in muscles of McArdle's patients in vivo appears feasible, preferably with the use of an adeno-associated viral vector.Entities:
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Year: 1999 PMID: 10522901 DOI: 10.1212/wnl.53.6.1352
Source DB: PubMed Journal: Neurology ISSN: 0028-3878 Impact factor: 9.910