Understanding dystrophinopathies: an inventory of the structural and functional consequences of the absence of dystrophin in muscles of the mdx mouse.
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Changes in mechanosensitive channel gating following mechanical stimulation in skeletal muscle myotubes from the mdx mouseWidespread muscle expression of an AAV9 human mini-dystrophin vector after intravenous injection in neonatal dystrophin-deficient dogs.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trialsCa(2+) influx and opening of Ca(2+)-activated K(+) channels in muscle fibers from control and mdx mice.Intramembrane charge movement and L-type calcium current in skeletal muscle fibers isolated from control and mdx mice.Biglycan recruits utrophin to the sarcolemma and counters dystrophic pathology in mdx miceCytoplasmic gamma-actin contributes to a compensatory remodeling response in dystrophin-deficient muscleBone is functionally impaired in dystrophic mice but less so than skeletal muscle.Dose response in rodents and nonhuman primates after hydrodynamic limb vein delivery of naked plasmid DNA.Magnetic Resonance Assessment of Hypertrophic and Pseudo-Hypertrophic Changes in Lower Leg Muscles of Boys with Duchenne Muscular Dystrophy and Their Relationship to Functional Measurements.Human circulating AC133(+) stem cells restore dystrophin expression and ameliorate function in dystrophic skeletal muscle.Skeletal muscle function: role of ionic changes in fatigue, damage and disease.The decrease of expression of ryanodine receptor sub-type 2 is reversed by gentamycin sulphate in vascular myocytes from mdx mice.Mechanisms of stretch-induced muscle damage in normal and dystrophic muscle: role of ionic changes.Intact satellite cells lead to remarkable protection against Smn gene defect in differentiated skeletal muscle.Skeletal muscle repair by adult human mesenchymal stem cells from synovial membrane.The force-temperature relationship in healthy and dystrophic mouse diaphragm; implications for translational study design.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Progress in gene therapy of dystrophic heart disease.A necrotic stimulus is required to maximize matrix-mediated myogenesis in miceDystrophic skeletal muscle fibers display alterations at the level of calcium microdomains.Comparative Genomics of X-linked Muscular Dystrophies: The Golden Retriever ModelHeregulin ameliorates the dystrophic phenotype in mdx mice.Canine models of Duchenne muscular dystrophy and their use in therapeutic strategies.The paradox of muscle hypertrophy in muscular dystrophy.Leaky ryanodine receptors delay the activation of store overload-induced Ca2+ release, a mechanism underlying malignant hyperthermia-like events in dystrophic muscle.Global/temporal gene expression in diaphragm and hindlimb muscles of dystrophin-deficient (mdx) mice.Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers.Sternohyoid muscle fatigue properties of dy/dy dystrophic mice, an animal model of merosin-deficient congenital muscular dystrophy.Levels of S100B protein drive the reparative process in acute muscle injury and muscular dystrophy.In situ measurements of calpain activity in isolated muscle fibres from normal and dystrophin-lacking mdx mice.Depolarization-induced contraction and SR function in mechanically skinned muscle fibers from dystrophic mdx mice.Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice.Decreased expression of ryanodine receptors alters calcium-induced calcium release mechanism in mdx duodenal myocytes.The action potential-evoked sarcoplasmic reticulum calcium release is impaired in mdx mouse muscle fibres.Effects of stretch-activated channel blockers on [Ca2+]i and muscle damage in the mdx mouse.Comparison of the myoplasmic calcium transient elicited by an action potential in intact fibres of mdx and normal mice.Propagation in the transverse tubular system and voltage dependence of calcium release in normal and mdx mouse muscle fibres.EDL and soleus muscles of the C57BL6J/dy2j laminin-alpha 2-deficient dystrophic mouse are not vulnerable to eccentric contractions.Dissection of temporal gene expression signatures of affected and spared muscle groups in dystrophin-deficient (mdx) mice.
P2860
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P2860
Understanding dystrophinopathies: an inventory of the structural and functional consequences of the absence of dystrophin in muscles of the mdx mouse.
description
1999 nî lūn-bûn
@nan
1999 թուականի Հոկտեմբերին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի հոտեմբերին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@ast
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@en
type
label
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@ast
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@en
prefLabel
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@ast
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@en
P356
P1476
Understanding dystrophinopathi ...... n in muscles of the mdx mouse.
@en
P2093
P2888
P304
P356
10.1023/A:1005545325254
P577
1999-10-01T00:00:00Z
P6179
1030940366