Association of dystrophin-related protein with dystrophin-associated proteins in mdx mouse muscle.

Twitch and tetanus in mdx mouse muscle.

Caspase-12 ablation preserves muscle function in the mdx mouse.

Muscle damage in mdx mice.

Galectin-1 Protein Therapy Prevents Pathology and Improves Muscle Function in the mdx Mouse Model of Duchenne Muscular Dystrophy.

A mathematical model of skeletal muscle disease and immune response in the mdx mouse.

Neuromuscular transmission in the mdx mouse.

Dystrophin-associated proteins are greatly reduced in skeletal muscle from mdx mice.

X-irradiation improves mdx mouse muscle as a model of myofiber loss in DMD.

Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy.

Developmental effects on the concentration of actin message in mdx and wild-type mouse muscle.

Immuno-electron-microscopic localization of basic fibroblast growth factor in the dystrophic mdx mouse masseter muscle.

Protein turnover is elevated in muscle of mdx mice in vivo.

Myofibrillar misalignment correlated to triad disappearance of mdx mouse gastrocnemius muscle probed by SHG microscopy.

Mechanical Overloading Increases Maximal Force and Reduces Fragility in Hind Limb Skeletal Muscle from Mdx Mouse.

Fiber regeneration is not persistent in dystrophic (MDX) mouse skeletal muscle.

A noninvasive procedure to detect muscle weakness in the mdx mouse.

Contractile properties and susceptibility to exercise-induced damage of normal and mdx mouse tibialis anterior muscle.

Decreased osmotic stability of dystrophin-less muscle cells from the mdx mouse.

Dystropathology increases energy expenditure and protein turnover in the mdx mouse model of duchenne muscular dystrophy.

Exercise increases utrophin protein expression in the mdx mouse model of Duchenne muscular dystrophy.

Alterations of protein degradation and 2-D protein pattern in muscle cells of MDX and DMD origin.

Overexpression of Id protein inhibits the muscle differentiation program: in vivo association of Id with E2A proteins.

Dysfunctional muscle and liver glycogen metabolism in mdx dystrophic mice.

suppression of the mouse mdx phenotype in vivo.

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Twitch and tetanus in mdx mouse muscle.

Caspase-12 ablation preserves muscle function in the mdx mouse.

Muscle damage in mdx mice.

Galectin-1 Protein Therapy Prevents Pathology and Improves Muscle Function in the mdx Mouse Model of Duchenne Muscular Dystrophy.

A mathematical model of skeletal muscle disease and immune response in the mdx mouse.

Neuromuscular transmission in the mdx mouse.

Dystrophin-associated proteins are greatly reduced in skeletal muscle from mdx mice.

X-irradiation improves mdx mouse muscle as a model of myofiber loss in DMD.

Increased plasma lipid levels exacerbate muscle pathology in the mdx mouse model of Duchenne muscular dystrophy.

Developmental effects on the concentration of actin message in mdx and wild-type mouse muscle.

Immuno-electron-microscopic localization of basic fibroblast growth factor in the dystrophic mdx mouse masseter muscle.

Protein turnover is elevated in muscle of mdx mice in vivo.

Myofibrillar misalignment correlated to triad disappearance of mdx mouse gastrocnemius muscle probed by SHG microscopy.

Mechanical Overloading Increases Maximal Force and Reduces Fragility in Hind Limb Skeletal Muscle from Mdx Mouse.

Fiber regeneration is not persistent in dystrophic (MDX) mouse skeletal muscle.

A noninvasive procedure to detect muscle weakness in the mdx mouse.

Contractile properties and susceptibility to exercise-induced damage of normal and mdx mouse tibialis anterior muscle.

Decreased osmotic stability of dystrophin-less muscle cells from the mdx mouse.

Dystropathology increases energy expenditure and protein turnover in the mdx mouse model of duchenne muscular dystrophy.

Exercise increases utrophin protein expression in the mdx mouse model of Duchenne muscular dystrophy.

Alterations of protein degradation and 2-D protein pattern in muscle cells of MDX and DMD origin.

Overexpression of Id protein inhibits the muscle differentiation program: in vivo association of Id with E2A proteins.

Dysfunctional muscle and liver glycogen metabolism in mdx dystrophic mice.

suppression of the mouse mdx phenotype in vivo.

Association of dystrophin-related protein with dystrophin-associated proteins in mdx mouse muscle.

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