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Previous Volume 352:2413-2423 June 9, 2005 Number 23 Next

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Calpains are Ca²⁺-dependent cysteine proteases (proteolytic enzymes with cysteine in the catalytic site) that modulate cellular function. In humans, 14 independent genes encode members of the calpain superfamily. Some calpain proteases are confined to specific tissues, whereas others are ubiquitous. Tissue-specific calpains have been implicated in diabetes, cataracts, multiple sclerosis, cancer, Duchenne's muscular dystrophy, and Alzheimer's disease and are known to cause at least one disorder, autosomal recessive limb-girdle muscular dystrophy type 2A (LGMD2A). We will review recent findings on the role of the calpain superfamily in these disorders, focusing on LGMD2A, the most extensively characterized human calpainopathy.

Properties of Calpains

Two . . . [Full Text of this Article]

Calpain-Associated Diseases

Limb-Girdle Muscular Dystrophy Type 2A

            Molecular Mechanisms

            Clinical Features

            CAPN3 Mutations, CAPN3 Protein Analysis, and Diagnostic Applications

            Genotype–Phenotype Correlation

            Location of the Second CAPN3 Mutation

Type 2 Diabetes

Alzheimer's Disease

Cataracts

Calpain Inhibitors

Source Information

From the Human Genome Research Center, Departamento de Biologia, Instituto de Biociências; Universidade de São Paulo, São Paulo.

Address reprint requests to Dr. Zatz at the Departamento de Biologia, Instituto de Biociências, Universidade de São Paulo, Rua do Matão 277, Cidade Universitária, CEP 05508-900, São Paulo, Brazil, or at mayazatz@usp.br.

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