Expression of a NOS transgene in dystrophin-deficient muscle reduces muscle membrane damage without increasing the expression of membrane-associated cytoskeletal proteins.
about
Primary role of functional ischemia, quantitative evidence for the two-hit mechanism, and phosphodiesterase-5 inhibitor therapy in mouse muscular dystrophyNutraceuticals and Their Potential to Treat Duchenne Muscular Dystrophy: Separating the Credible from the ConjectureAttempting to Compensate for Reduced Neuronal Nitric Oxide Synthase Protein with Nitrate Supplementation Cannot Overcome Metabolic Dysfunction but Rather Has Detrimental Effects in Dystrophin-Deficient mdx Muscle.Muscle exercise in limb girdle muscular dystrophies: pitfall and advantages.Sarcolemmal targeting of nNOSμ improves contractile function of mdx muscle.Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Loss of positive allosteric interactions between neuronal nitric oxide synthase and phosphofructokinase contributes to defects in glycolysis and increased fatigability in muscular dystrophy.EUK-134 ameliorates nNOSμ translocation and skeletal muscle fiber atrophy during short-term mechanical unloading.Exacerbation of pathology by oxidative stress in respiratory and locomotor muscles with Duchenne muscular dystrophy.Evaluation of the therapeutic utility of phosphodiesterase 5A inhibition in the mdx mouse model of duchenne muscular dystrophy.Cell-matrix interactions in muscle disease.Contribution of oxidative stress to pathology in diaphragm and limb muscles with Duchenne muscular dystrophy.Functional muscle ischemia in Duchenne and Becker muscular dystrophy.Fat deposition and accumulation in the damaged and inflamed skeletal muscle: cellular and molecular players.Redox homeostasis and age-related deficits in neuromuscular integrity and function.Therapeutic strategies to address neuronal nitric oxide synthase deficiency and the loss of nitric oxide bioavailability in Duchenne Muscular Dystrophy.Sodium nitrate alleviates functional muscle ischaemia in patients with Becker muscular dystrophy.Skeletal Muscle Metabolism in Duchenne and Becker Muscular Dystrophy-Implications for Therapies.
P2860
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P2860
Expression of a NOS transgene in dystrophin-deficient muscle reduces muscle membrane damage without increasing the expression of membrane-associated cytoskeletal proteins.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh-hant
name
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@en
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@nl
type
label
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@en
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@nl
prefLabel
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@en
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@nl
P1476
Expression of a NOS transgene ...... ociated cytoskeletal proteins.
@en
P2093
James G Tidball
Michelle Wehling-Henricks
P304
P356
10.1016/J.YMGME.2004.06.006
P577
2004-08-01T00:00:00Z