Abstract
Caveolins, the principle component of flask-shaped invaginations of the plasma membrane known as caveolae, play important roles in signal transduction and vesicular trafficking events by acting as scaffolding proteins. Heterozygous mutation of caveolin-3, the muscle-specific isoform of caveolins, results in autosomal dominant limb-girdle muscular dystrophy (LGMD1C), however, molecular mechanism of this disease has remained elusive. We previously generated transgenic mice overexpressing the P104L mutant caveolin-3 as a model of LGMD1C, which showed a myopathy characterized by severe skeletal muscle atrophy and loss and cytoplasmic mislocalization of caveolin-3.
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