Malformed mdx myofibers have normal cytoskeletal architecture yet altered EC coupling and stress-induced Ca2+ signaling.
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Critical Role of Intracellular RyR1 Calcium Release Channels in Skeletal Muscle Function and DiseaseAlternating bipolar field stimulation identifies muscle fibers with defective excitability but maintained local Ca(2+) signals and contraction.Altered nuclear dynamics in MDX myofibers.Incidence and severity of myofiber branching with regeneration and aging.Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle.Human skeletal muscle xenograft as a new preclinical model for muscle disordersEccentric exercise in aging and diseased skeletal muscle: good or bad?A new function for odorant receptors: MOR23 is necessary for normal tissue repair in skeletal muscle.Physiological characterization of muscle strength with variable levels of dystrophin restoration in mdx mice following local antisense therapy.Engraftment potential of dermal fibroblasts following in vivo myogenic conversion in immunocompetent dystrophic skeletal muscleThe role of proteases in excitation-contraction coupling failure in muscular dystrophy.Temporal changes in magnetic resonance imaging in the mdx mouseRecovery of altered neuromuscular junction morphology and muscle function in mdx mice after injuryAssessment of calcium sparks in intact skeletal muscle fibersUse of BODIPY (493/503) to visualize intramuscular lipid droplets in skeletal muscle.SERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.Pre- and postsynaptic changes in the neuromuscular junction in dystrophic mice.Abnormalities in brain structure and biochemistry associated with mdx mice measured by in vivo MRI and high resolution localized (1)H MRS.Structural and functional evaluation of branched myofibers lacking intermediate filamentsEarly metabolic changes measured by 1H MRS in healthy and dystrophic muscle after injuryNanospan, an alternatively spliced isoform of sarcospan, localizes to the sarcoplasmic reticulum in skeletal muscle and is absent in limb girdle muscular dystrophy 2F.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Decrease of myofiber branching via muscle-specific expression of the olfactory receptor mOR23 in dystrophic muscle leads to protection against mechanical stress.Using a novel coculture model to dissect the role of intramuscular lipid load on skeletal muscle insulin responsiveness under reduced estrogen conditions.Dysferlin stabilizes stress-induced Ca2+ signaling in the transverse tubule membrane.Proteomics of skeletal muscle differentiation, neuromuscular disorders and fiber aging.The dystrophin-glycoprotein complex in the prevention of muscle damage.Chaperoning heat shock proteins: proteomic analysis and relevance for normal and dystrophin-deficient muscle.Myofibrillar misalignment correlated to triad disappearance of mdx mouse gastrocnemius muscle probed by SHG microscopy.Drug Discovery of Therapies for Duchenne Muscular Dystrophy.Establishment of a human skeletal muscle-derived cell line: biochemical, cellular and electrophysiological characterization.Myofiber branching rather than myofiber hyperplasia contributes to muscle hypertrophy in mdx mice.Disruption of action potential and calcium signaling properties in malformed myofibers from dystrophin-deficient mice.Detection of calcium sparks in intact and permeabilized skeletal muscle fibers.PGC-1α gene transfer improves muscle function in dystrophic muscle following prolonged disease progress.Effects of in vivo injury on the neuromuscular junction in healthy and dystrophic muscles.Imaging Analysis of the Neuromuscular Junction in Dystrophic Muscle.Brain and heart magnetic resonance imaging/spectroscopy in duchenne muscular dystrophy.Combined XIL-6R and urocortin-2 treatment restores MDX diaphragm muscle force.Nanoscale remodeling of ryanodine receptor cluster size underlies cerebral microvascular dysfunction in Duchenne muscular dystrophy
P2860
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P2860
Malformed mdx myofibers have normal cytoskeletal architecture yet altered EC coupling and stress-induced Ca2+ signaling.
description
article científic
@ca
article scientifique
@fr
articolo scientifico
@it
artigo científico
@pt
bilimsel makale
@tr
scientific article published on 15 July 2009
@en
vedecký článok
@sk
vetenskaplig artikel
@sv
videnskabelig artikel
@da
vědecký článek
@cs
name
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@en
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@nl
type
label
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@en
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@nl
prefLabel
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@en
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@nl
P2093
P2860
P1476
Malformed mdx myofibers have n ...... stress-induced Ca2+ signaling.
@en
P2093
Christopher W Ward
Luke Michaelson
Richard M Lovering
P2860
P304
P356
10.1152/AJPCELL.00087.2009
P577
2009-07-15T00:00:00Z