Elevated subsarcolemmal Ca2+ in mdx mouse skeletal muscle fibers detected with Ca2+-activated K+ channels.
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Calcium antagonists for Duchenne muscular dystrophyCalcium antagonists for Duchenne muscular dystrophyBrain dystrophin-glycoprotein complex: persistent expression of beta-dystroglycan, impaired oligomerization of Dp71 and up-regulation of utrophins in animal models of muscular dystrophyAlteration of excitation-contraction coupling mechanism in extensor digitorum longus muscle fibres of dystrophic mdx mouse and potential efficacy of taurineChanges in mechanosensitive channel gating following mechanical stimulation in skeletal muscle myotubes from the mdx mouseGestational diabetes is characterized by reduced mitochondrial protein expression and altered calcium signaling proteins in skeletal musclePrimary Murine Myotubes as a Model for Investigating Muscular DystrophyProteomic profiling of antisense-induced exon skipping reveals reversal of pathobiochemical abnormalities in dystrophic mdx diaphragm.Convergent regulation of skeletal muscle Ca2+ channels by dystrophin, the actin cytoskeleton, and cAMP-dependent protein kinase.Ca(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.Debio-025 is more effective than prednisone in reducing muscular pathology in mdx mice.Orai1 mediates exacerbated Ca(2+) entry in dystrophic skeletal muscleLengthening-contractions in isolated myocardium impact force development and worsen cardiac contractile function in the mdx mouse model of muscular dystrophy.Sarcoplasmic reticulum Ca2+ permeation explored from the lumen side in mdx muscle fibers under voltage controlSoluble miniagrin enhances contractile function of engineered skeletal muscle.Enhanced Na+/H+ exchange activity contributes to the pathogenesis of muscular dystrophy via involvement of P2 receptors.Characterization and Functional Analysis of Extracellular Vesicles and Muscle-Abundant miRNAs (miR-1, miR-133a, and miR-206) in C2C12 Myocytes and mdx MiceProfiling 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.Proteomics reveals drastic increase of extracellular matrix proteins collagen and dermatopontin in the aged mdx diaphragm model of Duchenne muscular dystrophyAltered calcium pump and secondary deficiency of gamma-sarcoglycan and microspan in sarcoplasmic reticulum membranes isolated from delta-sarcoglycan knockout mice.Cancer cachexia causes skeletal muscle damage via transient receptor potential vanilloid 2-independent mechanisms, unlike muscular dystrophyAnimal models of muscular dystrophyGenetic and pharmacologic inhibition of mitochondrial-dependent necrosis attenuates muscular dystrophy.Wasting mechanisms in muscular dystrophy.Comparative proteomic profiling of soleus, extensor digitorum longus, flexor digitorum brevis and interosseus muscles from the mdx mouse model of Duchenne muscular dystrophyCalcium influx is sufficient to induce muscular dystrophy through a TRPC-dependent mechanism.Chaperoning heat shock proteins: proteomic analysis and relevance for normal and dystrophin-deficient muscle.Drug Discovery of Therapies for Duchenne Muscular Dystrophy.Mitochondrial Ca(2+) uptake in skeletal muscle health and disease.Na+ dysregulation coupled with Ca2+ entry through NCX1 promotes muscular dystrophy in mice.STIM1 signalling controls store-operated calcium entry required for development and contractile function in skeletal muscleBcl-2 overexpression prevents calcium overload and subsequent apoptosis in dystrophic myotubes.Drastic reduction of sarcalumenin in Dp427 (dystrophin of 427 kDa)-deficient fibres indicates that abnormal calcium handling plays a key role in muscular dystrophy.Involvement of TRPC in the abnormal calcium influx observed in dystrophic (mdx) mouse skeletal muscle fibers.Negative modulation of inositol 1,4,5-trisphosphate type 1 receptor expression prevents dystrophin-deficient muscle cells death.Characterization of K(+) currents using an in situ patch clamp technique in body wall muscle cells from Caenorhabditis elegans.Isoprenaline-stimulated differential adrenergic response of K+ channels in skeletal muscle under hypokalaemic conditions.Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice.
P2860
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P2860
Elevated subsarcolemmal Ca2+ in mdx mouse skeletal muscle fibers detected with Ca2+-activated K+ channels.
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
Elevated subsarcolemmal Ca2+ i ...... th Ca2+-activated K+ channels.
@ast
Elevated subsarcolemmal Ca2+ i ...... th Ca2+-activated K+ channels.
@en
type
label
Elevated subsarcolemmal Ca2+ i ...... th Ca2+-activated K+ channels.
@ast
Elevated subsarcolemmal Ca2+ i ...... th Ca2+-activated K+ channels.
@en
prefLabel
Elevated subsarcolemmal Ca2+ i ...... th Ca2+-activated K+ channels.
@ast
Elevated subsarcolemmal Ca2+ i ...... th Ca2+-activated K+ channels.
@en
P2860
P356
P1476
Elevated subsarcolemmal Ca2+ i ...... ith Ca2+-activated K+ channels
@en
P2093
P2860
P304
P356
10.1073/PNAS.97.9.4950
P407
P50
P577
2000-04-01T00:00:00Z