Phenotypic Behavior of Caveolin-3 Mutations That Cause Autosomal Dominant Limb Girdle Muscular Dystrophy (LGMD-1C)

descriptionPublicationkeyboard_double_arrow_right Article 01 Sep 1999 English Publisher:Elsevier BVJournal:Journal of Biological Chemistry, volume 274, pages 25,632-25,641 (issn: 0021-9258,

Authors: Ferruccio Galbiati; Daniela Volonté; Carlo Minetti; Jeffrey B. Chu; Michael P. Lisanti;

doi: 10.1074/jbc.274.36.25632

Phenotypic Behavior of Caveolin-3 Mutations That Cause Autosomal Dominant Limb Girdle Muscular Dystrophy (LGMD-1C)

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University of Genoa
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Albert Einstein College of Medicine
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Yeshiva University
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10 Research products, page 1 of 1

Limb-girdle muscular dystrophy (LGMD-1C) mutants of caveolin-3 undergo ubiquitination and proteasomal degradation. Treatment with proteasomal inhibitors blocks the dominant negative effect of LGMD-1C mutanta and rescues wild-type caveolin-3.
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Limb-girdle Muscular Dystrophy (LGMD-1C) Mutants of Caveolin-3 Undergo Ubiquitination and Proteasomal Degradation
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Phenotypic behavior of caveolin-3 mutations that cause autosomal dominant limb girdle muscular dystrophy (LGMD-1C). Retention of LGMD-1C caveolin-3 mutants within the golgi complex.
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Caveolin-3 Null Mice Show a Loss of Caveolae, Changes in the Microdomain Distribution of the Dystrophin-Glycoprotein Complex, and T-tubule Abnormalities
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A caveolin-3 mutant that causes limb girdle muscular dystrophy type 1C disrupts Src localization and activity and induces apoptosis in skeletal myotubes
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Modulation of Myoblast Fusion by Caveolin-3 in Dystrophic Skeletal Muscle Cells: Implications for Duchenne Muscular Dystrophy and Limb-Girdle Muscular Dystrophy-1C
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Impairment of Caveolae Formation and T-System Disorganization in Human Muscular Dystrophy with Caveolin-3 Deficiency
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