Localization of Muscle Gene Products in Nuclear Domains: Does this Constitute a Problem for Myoblast Therapy?
A question of major interest in considering myoblast therapy is whether the gene product dystrophin, provided by the introduced myoblasts, can contribute to the function of the myofiber into which the cells fuse. As shown in several papers in this volume, there is now ample evidence that injected myoblasts can fuse with myofibers and produce dystrophin, but the question of whether that dystrophin can restore muscle function still remains. In this regard, a major consideration is whether dystrophin can gain access to distant sites within the myofiber or remains localized in the vicinity of the nucleus that encoded it.
KeywordsPolyethylene Glycol Creatine Fluorescein Isothiocyanate
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- 11.Gearhart, J.D. and B. Mintz, Clonal origins of somites and their muscle derivatives; evidence from allophenic mice,Develop. Biol. 29: 27 (1972).Google Scholar
- 12.Hausmanowa- Petrusewicz, I., I. Niebroj- Dobosz, J. Borkowska, E. Lukasik and D. Liszewska-Pfejfer, Carrier detection in Duchenne dystrophy in: “Pathogenesis of Human Muscular Dystrophies,” L.P. Rowland, ed., Excerpta Medica, Oxford (1977).Google Scholar
- 16.Webster, C., L. Silberstein, A.P. Hays and H.M. Blau, Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy, Cell, 52: 502 (1988).Google Scholar