Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice.
about
Inhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expressionP2RX7 purinoceptor: a therapeutic target for ameliorating the symptoms of duchenne muscular dystrophyThe inotropic peptide βARKct improves βAR responsiveness in normal and failing cardiomyocytes through G(βγ)-mediated L-type calcium current disinhibition.L-type Ca2+ channel function is linked to dystrophin expression in mammalian muscleRapid Ca2+ flux through the transverse tubular membrane, activated by individual action potentials in mammalian skeletal muscle.Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle.Functional expression of transgenic 1sDHPR channels in adult mammalian skeletal muscle fibres.Genetic inhibition of PKA phosphorylation of RyR2 prevents dystrophic cardiomyopathy.Phosphorylation within the cysteine-rich region of dystrophin enhances its association with β-dystroglycan and identifies a potential novel therapeutic target for skeletal muscle wasting.Quadriceps myopathy caused by skeletal muscle-specific ablation of β(cyto)-actinNitrosative stress elicited by nNOSµ delocalization inhibits muscle force in dystrophin-null miceRecombinant adeno-associated viral (rAAV) vectors as therapeutic tools for Duchenne muscular dystrophy (DMD).Mutation of delta-sarcoglycan is associated with Ca(2+) -dependent vascular remodeling in the Syrian hamster.Unloaded speed of shortening in voltage-clamped intact skeletal muscle fibers from wt, mdx, and transgenic minidystrophin mice using a novel high-speed acquisition system.Dysferlin stabilizes stress-induced Ca2+ signaling in the transverse tubule membrane.Cardiac and respiratory dysfunction in Duchenne muscular dystrophy and the role of second messengers.P2X7 purinoceptor alterations in dystrophic mdx mouse muscles: relationship to pathology and potential target for treatmentRegulation of TRPC1 and TRPC4 cation channels requires an alpha1-syntrophin-dependent complex in skeletal mouse myotubes.Hybrid spectrin type repeats produced by exon-skipping in dystrophin.Voltage-controlled Ca2+ release and entry flux in isolated adult muscle fibres of the mouse.The action potential-evoked sarcoplasmic reticulum calcium release is impaired in mdx mouse muscle fibres.Acute failure of action potential conduction in mdx muscle reveals new mechanism of contraction-induced force loss.Effects of stretch-activated channel blockers on [Ca2+]i and muscle damage in the mdx mouse.Quantitative calcium measurements in subcellular compartments of Plasmodium falciparum-infected erythrocytes.Propagation in the transverse tubular system and voltage dependence of calcium release in normal and mdx mouse muscle fibres.Electromyographic studies in mdx and wild-type C57 mice.Enhanced muscle shortening and impaired Ca2+ channel function in an acute septic myopathy model.
P2860
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P2860
Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice.
description
2003 nî lūn-bûn
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2003年の論文
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2003年学术文章
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2003年学术文章
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2003年学术文章
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@zh-hans
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name
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice.
@en
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice.
@nl
type
label
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice.
@en
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice.
@nl
prefLabel
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice.
@en
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice.
@nl
P2093
P2860
P1476
Mini-dystrophin restores L-typ ...... muscle of transgenic mdx mice
@en
P2093
J M Gillis
J S Chamberlain
R H A Fink
P2860
P304
P356
10.1113/JPHYSIOL.2003.054213
P407
P577
2003-10-31T00:00:00Z