Suppression of revertant fibers in mdx mice by expression of a functional dystrophin

Human Molecular Genetics

Volumn 10, Issue 24, 2001, Pages 2745-2750

  Crawford, Gregory E ^a   Lu, Qi Long ^b   Partridge, Terry A ^b   Chamberlain, Jeffrey S ^a,c,d  

^a UNIVERSITY OF MICHIGAN   (United States)

^b HAMMERSMITH HOSPITAL   (United Kingdom)

^c UNIVERSITY OF WASHINGTON   (United States)

^d UNIVERSITY OF WASHINGTON SCHOOL OF MEDICINE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DYSTROPHIN; RNA;

ANIMAL EXPERIMENT; ANIMAL MODEL; ANIMAL TISSUE; ARTICLE; CONTROLLED STUDY; DUCHENNE MUSCULAR DYSTROPHY; GENE FUNCTION; GENE LOSS; GENE OVEREXPRESSION; GENETIC CODE; GENETIC SELECTION; MOUSE; NEWBORN; NONHUMAN; PATHOLOGY; PRIORITY JOURNAL; PROTEIN EXPRESSION; REVERTANT; TRANSGENE; TRANSGENIC MOUSE;

ANIMALIA; MUS MUSCULUS;

EID: 0035891875     PISSN: 09646906     EISSN: None     Source Type: Journal    
DOI: 10.1093/hmg/10.24.2745     Document Type: Article

References (33)

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7. Contraction-induced injury to single permeabilized muscle fibers from mdx, transgenic mdx and control mice
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15. Revertant fibres: A possible genetic therapy for Duchenne muscular dystrophy?
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19. Polymerase chain reaction fiber analysis and somatic mosaicism in autopsied tissue from a man with Duchenne muscular dystrophy
20. Exon skipping and translation in patients with frameshift deletions in the dystrophin gene
21. Assembly of the dystrophin-associated protein complex does not require the dystrophin COOH-terminal domain
22. Expression of full-length and truncated dystrophin mini-genes in transgenic mdx mice
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25. Dp71 can restore the dystrophin-associated glycoprotein complex in muscle but fails to prevent dystrophy
26. New mdx mutation disrupts expression of muscle and nonmuscle isoforms of dystrophin
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28. Rescue of dystrophin expression in mdx mouse muscle by RNA/DNA oligonucleotides
29. Modification of splicing in the dystrophin gene in cultured mdx muscle cells by antisense oligoribonucleotides
30. Transgenic mdx mice expressing dystrophin with a deletion in the actin-binding domain display a 'mild becker' phenotype
31. A b2 repeat insertion generates alternate structures of the mouse muscle γ-phosphorylase kinase gene
32. Prevention of dystrophic pathology in mdx mice by a truncated dystrophin isoform