Molecular and Cell Biology of Muscular Dystrophy by Anthony P. Monaco (auth.), Terence Partridge (eds.)

By Anthony P. Monaco (auth.), Terence Partridge (eds.)

Molecular and telephone Biology of Muscular Dystrophy provides a chain of bills of varied facets of the notable step forward which has been completed in our figuring out of the Duchenne/Becker muscular dystrophies and of the implications and ramifications of this breakthrough.

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Neuromuscular Disorders, 2,41-5. S. et al. (1989) Familial X-linked myalgia and cramps. Neurology, 39, 1277-80. R. (1879). Pseudo-hypertrophic muscular paralysis. A clinical lecture, J & A Churchill. , Halliday, W. and Wrogemann, K. (1991) Three years' experience with neonatal screening for DuchennelBecker muscular dystrophy: Gene analysis, gene expression and phenotype prediction. Am. ]. Med. , 39, 68-75. , Abbs, S. et al. (1989) Correlation of clinical and deletion data in Duchenne and Becker muscular dystrophy.

J. Hum. , 46, 682-95. P. M. (1990) Identification of a chromosome 6 encoded dystrophin related protein. J. Bioi. , 265, 16717-20. , Chafey, P. et al. (1991) Immunolocalization and developmental expression of DRP in skeletal muscle. Neuromuscular Disorders, 1, 185-94. E. et al. suppression in Duchenne muscular dystrophy (DMD): evidence supporting a frame restoring mechanism in rare dystrophin positive fibers. Am J. Hum. , 50, 950-9. ]. et al. (1987). Complete cloning of the Duchenne muscular dystrophy (DMD) eDNA and preliminary genomic organization of the DMD gene in normal and affected individuals.

While most patients with these common deletions have relatively mild phenotypes (bottom), single patients can be found with the same exon deletions and relatively severe phenotypes (top). This shows the clinical variability in Becker dystrophy which may be due to extragenic factors, or the unknown effect of specific deletions on mRNA splicing or stability. Less severe phenotypes More severe phenotypes REFERENCES important for dystrophin structure and function that does the integrity of the central rod domain.

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