Related references
Note: Only part of the references are listed.Pathogenity of some limb girdle muscular dystrophy mutations can result from reduced anchorage to myofibrils and altered stability of calpain 3
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Endogenous Calpain-3 Activation Is Primarily Governed by Small Increases in Resting Cytoplasmic [Ca2+] and Is Not Dependent on Stretch
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JOURNAL OF BIOLOGICAL CHEMISTRY (2009)
cDNA analyses of CAPN3 enhance mutation detection and reveal a low prevalence of LGMD2A patients in Denmark
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Calpain 3 is a modulator of the dysferlin protein complex in skeletal muscle
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Multiple molecular interactions implicate the connectin/titin N2A region as a modulating scaffold for p94/calpain 3 activity in skeletal muscle
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A third of LGMD2A biopsies have normal calpain 3 proteolytic activity as determined by an in vitro assay
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LGMD2I presenting with a characteristic Duchenne or Becker muscular dystrophy phenotype
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Diagnostic value of muscle MRI in differentiating LGMD2I from other LGMDs
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Novel mutations in the calpain 3 gene in Germany
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Null mutation of calpain 3 (p94) in mice causes abnormal sarcomere formation in vivo and in vitro
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HUMAN MOLECULAR GENETICS (2004)
Loss of calpain-3 autocatalytic activity in LGMD2A patients with normal protein expression
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AMERICAN JOURNAL OF PATHOLOGY (2003)
Muscle pathology in dysferlin deficiency
M Fanin et al.
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Reliability of hand-held dynamometry in spinal muscular atrophy
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MUSCLE & NERVE (2002)
Reference values of maximum isometric muscle force obtained in 270 children aged 4-16 years by hand-held dynamometry
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The expression of intermediate filament protein nestin as related to vimentin and desmin in regenerating skeletal muscle
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Mutations in calpain 3 associated with limb girdle muscular dystrophy: Analysis by molecular modeling and by mutation in m-calpain
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