Calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes.
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Mechanosensitive channel properties and membrane mechanics in mouse dystrophic myotubesBrain dystrophin-glycoprotein complex: persistent expression of beta-dystroglycan, impaired oligomerization of Dp71 and up-regulation of utrophins in animal models of muscular dystrophyDeficiency in Cardiac Dystrophin Affects the Abundance of the $\alpha$ -/ $\beta$ -Dystroglycan ComplexAn alpha-catulin homologue controls neuromuscular function through localization of the dystrophin complex and BK channels in Caenorhabditis elegansInhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expressionAlteration of excitation-contraction coupling mechanism in extensor digitorum longus muscle fibres of dystrophic mdx mouse and potential efficacy of taurineUse of imaging biomarkers to assess perfusion and glucose metabolism in the skeletal muscle of dystrophic mice.Comparative study of mesenchymal stem cells from C57BL/10 and mdx miceL-type Ca2+ channel function is linked to dystrophin expression in mammalian muscleProteomic profiling of antisense-induced exon skipping reveals reversal of pathobiochemical abnormalities in dystrophic mdx diaphragm.The dystrophin complex controls bk channel localization and muscle activity in Caenorhabditis elegans.Dexamethasone stimulates store-operated calcium entry and protein degradation in cultured L6 myotubes through a phospholipase A(2)-dependent mechanism.Increased store-operated Ca2+ entry in skeletal muscle with reduced calsequestrin-1 expression.Altered cross-bridge properties in skeletal muscle dystrophiesLong-term blocking of calcium channels in mdx mice results in differential effects on heart and skeletal muscleEffects of an immunosuppressive treatment in the GRMD dog model of Duchenne muscular dystrophy.Orai1 mediates exacerbated Ca(2+) entry in dystrophic skeletal muscleEffect of nutrient restriction and re-feeding on calpain family genes in skeletal muscle of channel catfish (Ictalurus punctatus)How Does the Ca(2+)-paradox Injury Induce Contracture in the Heart?-A Combined Study of the Intracellular Ca(2+) Dynamics and Cell Structures in Perfused Rat Hearts.The dystrophin-associated protein complex maintains muscle excitability by regulating Ca(2+)-dependent K(+) (BK) channel localization.Enhanced Na+/H+ exchange activity contributes to the pathogenesis of muscular dystrophy via involvement of P2 receptors.Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes.Profiling of age-related changes in the tibialis anterior muscle proteome of the mdx mouse model of dystrophinopathyA novel mechanism of myocyte degeneration involving the Ca2+-permeable growth factor-regulated channel.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Mechanosensitive TRPC1 channels promote calpain proteolysis of talin to regulate spinal axon outgrowthAnimal models of muscular dystrophyInhibition of iPLA2 β and of stretch-activated channels by doxorubicin alters dystrophic muscle function.Wasting mechanisms in muscular dystrophy.Leupeptin-based inhibitors do not improve the mdx phenotype.Skeletal muscle as a paradigm for regenerative biology and medicine.The roles of the dystrophin-associated glycoprotein complex at the synapseCalpain-mediated proteolysis of tropomodulin isoforms leads to thin filament elongation in dystrophic skeletal muscle.The dystrophin-glycoprotein complex in the prevention of muscle damage.Role of calpain in apoptosis.The physiological response of protease inhibition in dystrophic muscle.Chaperoning heat shock proteins: proteomic analysis and relevance for normal and dystrophin-deficient muscle.The role of mechanobiology in progression of rotator cuff muscle atrophy and degeneration.White striping and woody breast myopathies in the modern poultry industry: a review.Dystrophin deficiency leads to disturbance of LAMP1-vesicle-associated protein secretion.
P2860
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P2860
Calcium influx through calcium leak channels is responsible for the elevated levels of calcium-dependent proteolysis in dystrophic myotubes.
description
2000 nî lūn-bûn
@nan
2000年の論文
@ja
2000年論文
@yue
2000年論文
@zh-hant
2000年論文
@zh-hk
2000年論文
@zh-mo
2000年論文
@zh-tw
2000年论文
@wuu
2000年论文
@zh
2000年论文
@zh-cn
name
Calcium influx through calcium ...... olysis in dystrophic myotubes.
@en
type
label
Calcium influx through calcium ...... olysis in dystrophic myotubes.
@en
prefLabel
Calcium influx through calcium ...... olysis in dystrophic myotubes.
@en
P356
P1476
Calcium influx through calcium ...... olysis in dystrophic myotubes.
@en
P2093
J M Alderton
R A Steinhardt
P304
P356
10.1074/JBC.275.13.9452
P407
P577
2000-03-01T00:00:00Z