distal myopathies/protease

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Removal of the calpain 3 protease reverses the myopathology in a mouse model for titinopathies.

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The dominant tibial muscular dystrophy (TMD) and recessive limb-girdle muscular dystrophy 2J are allelic disorders caused by mutations in the C-terminus of titin, a giant sarcomeric protein. Both clinical presentations were initially identified in a large Finnish family and linked to a founder

Regulated proteolysis of p62/SQSTM1 enables differential control of autophagy and nutrient sensing.

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The multidomain scaffold protein p62 (also called sequestosome-1) is involved in autophagy, antimicrobial immunity, and oncogenesis. Mutations in SQSTM1, which encodes p62, are linked to hereditary inflammatory conditions such as Paget's disease of the bone, frontotemporal dementia (FTD),

[Muscle pathologic diagnosis--mechanism in muscle fiber degeneration].

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In various neuromuscular diseases, the most significant muscle degeneration is muscle fiber necrosis as seen in Duchenne muscular dystrophy (DMD). A certain membrane instability is probably responsible for muscle fiber necrosis, because defects in membrane proteins have been proposed to associate

[The genetic basis of muscle disease].

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BACKGROUND Our understanding of the genetic basis of muscle disease has grown dramatically over the last few years. Gene tests are now available for the diagnosis of several conditions and molecular research is providing greater understanding of pathogenesis. METHODS This article reviews some of

Computational Identification of Natural Product Leads that Inhibit Mast Cell Chymase: An Exclusive Plausible Treatment for Japanese Encephalitis.

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A recent research has identified chymase, a mast cell-specific protease as an exclusive novel therapeutic target to prevent Japanese encephalitis virus (JEV) induced encephalitis. Interestingly, JEV activates mast cell specific chymase during its penetration through blood brain barrier (BBB) which

Interactions with M-band titin and calpain 3 link myospryn (CMYA5) to tibial and limb-girdle muscular dystrophies.

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Mutations in the C terminus of titin, situated at the M-band of the striated muscle sarcomere, cause tibial muscular dystrophy (TMD) and limb-girdle muscular dystrophy (LGMD) type 2J. Mutations in the protease calpain 3 (CAPN3), in turn, lead to LGMD2A, and secondary CAPN3 deficiency in LGMD2J

Experimental chloroquine myopathy: morphological and biochemical studies.

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Morphological and biochemical studies were performed on the soleus muscles of rats receiving a daily intraperitoneal injection of 50 mg chloroquine chloride (CQ) per kilogram of body weight. Light microscopy showed mild to moderate variations in fiber size, numerous dense membranous bodies and

Mdm muscular dystrophy: interactions with calpain 3 and a novel functional role for titin's N2A domain.

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Human tibial muscular dystrophy and limb-girdle muscular dystrophy 2J are caused by mutations in the giant sarcomeric protein titin (TTN) adjacent to a binding site for the muscle-specific protease calpain 3 (CAPN3). Muscular dystrophy with myositis (mdm) is a recessive mouse mutation with severe

CAPN3-mediated processing of C-terminal titin replaced by pathological cleavage in titinopathy.

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Mutations in the extreme C-terminus of titin (TTN), situated in the sarcomeric M-band, cause tibial muscular dystrophy (TMD) and limb-girdle muscular dystrophy 2J (LGMD2J). The mutations ultimately cause a loss of C-terminal titin, including a binding site for the protease calpain 3 (CAPN3), and

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