myotonic dystrophy/protease

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Leukocyte protease activities in myotonic dystrophy: studies on effects of protease inhibitors.

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Neutral and acid protease activities inhibited by chymostatin, leupeptin, pepstatin and HgCl2 in mononuclear cells and granulocytes showed no significant differences between myotonic dystrophy patients and controls. These results suggest that chymotrypsin and cathepsin B and D activities are

Expression of late myogenic differentiation markers in sarcoplasmic masses of patients with myotonic dystrophy.

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Sarcoplasmic masses contain disorganized myofibrillar material and are a striking feature of myotonic dystrophy. However their significance is still unclear. Using immunocytochemistry we studied the expression of cytoskeletal proteins (desmin and vimentin), dystrophin, markers of myogenic

Muscle apoptosis in humans occurs in normal and denervated muscle, but not in myotonic dystrophy, dystrophinopathies or inflammatory disease.

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Recent data suggest that death of muscle cells during development and in selected pathological conditions occurs via apoptosis. We investigated the occurrence of apoptosis in normal and pathological human skeletal muscle, using in situ end-labeling (ISEL) to detect DNA fragmentation, and

Membrane defects in Duchenne dystrophy: protease affecting sarcoplasmic reticulum.

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Human muscle sarcoplasmic reticulum (SR) yields three major protein bands. The percent distribution of the mean values of the bands from 15 normal human muscles was 55.4, 14.6, and 30.0 for the 100, 55, and 45-kDa mass proteins, respectively. A mean distribution similar to that in normal muscle SR

Irreversible Activation of Rho-activated Kinases Resulted from Evolution of Proteolytic Sites within Disordered Regions in Coiled-coil Domain.

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Activation of Rho-associated protein kinase 1 (ROCK1) and myotonic dystrophy kinase-related CDC42-binding kinase alpha (MRCKα) by caspases during apoptosis in vertebrates represents a prototypical example of co-option of kinases by proteases. How caspases acquired the ability to control these

Features of modularly assembled compounds that impart bioactivity against an RNA target.

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Transcriptomes provide a myriad of potential RNAs that could be the targets of therapeutics or chemical genetic probes of function. Cell-permeable small molecules, however, generally do not exploit these targets, owing to the difficulty in the design of high affinity, specific small molecules

[Immunohistochemical localization of chymase; a mast cell marker and clinical significance in diseased human skeletal muscle].

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In the advanced stage of dystrophinopathy, cardiac dysfunction is a serious complication for prognosis. Recently, an angiotensin converting enzyme (ACE), which converts angiotensin (A) 1 to A 2, has been reported to be effective for cardiac insufficiency. The A 2 is produced more dominantly in the

Proteolytic enzyme activities in mononuclear cells and granulocytes of patients with various neurological disorders.

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Our studies showed a significantly increased neutral protease activity in mononuclear cells in patients with MS in relapse, active neuro-Behçet's disease, acute disseminated encephalomyelitis (ADEM) and polymyositis. Furthermore, in patients with ADEM there was a significant increase in the

Proteolytic enzyme activities of macrophages and lymphocytes in neurological diseases.

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Studies showed a significant decrease in the macrophage neutral protease and lymphocyte acid protease activities in patients with multiple sclerosis in remission, a significantly decreased neutral protease activity in macrophages in patients with myasthenia gravis and a significantly decreased acid

[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

Mecasermin rinfabate: insulin-like growth factor-I/insulin-like growth factor binding protein-3, mecaserimin rinfibate, rhIGF-I/rhIGFBP-3.

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Insmed is developing mecasermin rinfabate, a recombinant complex of insulin-like growth factor-I (rhIGF-I) and binding protein-3 (rhIGFBP-3) [insulin-like growth factor-I/insulin-like growth factor binding protein-3, rhIGF-I/rhIGFBP-3, SomatoKine], for a number of metabolic and endocrine

Increased rates of myofibrillar protein breakdown in muscle-wasting diseases.

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The excretion of endogenous creatinine and 3-methylhistidine by subjects with muscle diseases has been measured in order to assess muscle mass and fractional rates of myofibrillar protein degradation. Increases in the rates of myofibrillar protein breakdown were observed in all subjects with

Fibroblast-led collective invasion of carcinoma cells with differing roles for RhoGTPases in leading and following cells.

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Imaging of collectively invading cocultures of carcinoma cells and stromal fibroblasts reveals that the leading cell is always a fibroblast and that carcinoma cells move within tracks in the extracellular matrix behind the fibroblast. The generation of these tracks by fibroblasts is sufficient to

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