Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
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Maximum velocity of shortening in relation to myosin isoform composition in single fibres from human skeletal musclesMolecular genetic characterization of a developmentally regulated human perinatal myosin heavy chainExpression and DNA sequence analysis of a human embryonic skeletal muscle myosin heavy chain geneHuntingtin-associated protein (HAP1): discrete neuronal localizations in the brain resemble those of neuronal nitric oxide synthaseDesigning materials to direct stem-cell fateResveratrol and MyopathySIRT1: A Novel Target for the Treatment of Muscular DystrophiesMetabogenic and Nutriceutical Approaches to Address Energy Dysregulation and Skeletal Muscle Wasting in Duchenne Muscular DystrophyRescue of dystrophic skeletal muscle by PGC-1α involves a fast to slow fiber type shift in the mdx mouseMuscle-specific SIRT1 gain-of-function increases slow-twitch fibers and ameliorates pathophysiology in a mouse model of duchenne muscular dystrophyCREB is activated by muscle injury and promotes muscle regenerationAssociation of neuronal nitric oxide synthase (nNOS) with alpha1-syntrophin at the sarcolemmaNovel approach to meta-analysis of microarray datasets reveals muscle remodeling-related drug targets and biomarkers in Duchenne muscular dystrophyExpression of utrophin A mRNA correlates with the oxidative capacity of skeletal muscle fiber types and is regulated by calcineurin/NFAT signalingPregnancy-induced amelioration of muscular dystrophy phenotype in mdx mice via muscle membrane stabilization effect of glucocorticoidMetabolic dysfunction and altered mitochondrial dynamics in the utrophin-dystrophin deficient mouse model of duchenne muscular dystrophyDifferential association of syntrophin pairs with the dystrophin complexMuscular dystrophy begins early in embryonic development deriving from stem cell loss and disrupted skeletal muscle formationQuantitative NMRI and NMRS identify augmented disease progression after loss of ambulation in forearms of boys with Duchenne muscular dystrophy.A role for Insulin-like growth factor 2 in specification of the fast skeletal muscle fibre.Dystrophin deficiency in canine X-linked muscular dystrophy in Japan (CXMDJ) alters myosin heavy chain expression profiles in the diaphragm more markedly than in the tibialis cranialis muscle.Making fast-twitch dystrophic muscles bigger protects them from contraction injury and attenuates the dystrophic pathology.Physical training in boys with Duchenne Muscular Dystrophy: the protocol of the No Use is Disuse study.MicroRNA-486-dependent modulation of DOCK3/PTEN/AKT signaling pathways improves muscular dystrophy-associated symptomsEndogenous nitric oxide synthesis: biological functions and pathophysiology.Lymphocyte antigen Leu-19 as a molecular marker of regeneration in human skeletal muscle.Resveratrol induces expression of the slow, oxidative phenotype in mdx mouse muscle together with enhanced activity of the SIRT1-PGC-1α axis.iNOS ablation does not improve specific force of the extensor digitorum longus muscle in dystrophin-deficient mdx4cv mice.Circulating Muscle-specific miRNAs in Duchenne Muscular Dystrophy PatientsGenome-wide mapping of Sox6 binding sites in skeletal muscle reveals both direct and indirect regulation of muscle terminal differentiation by Sox6.Pharmacologic management of Duchenne muscular dystrophy: target identification and preclinical trialsAltered cross-bridge properties in skeletal muscle dystrophiesDifferences in aberrant expression and splicing of sarcomeric proteins in the myotonic dystrophies DM1 and DM2.Combined effect of AMPK/PPAR agonists and exercise training in mdx mice functional performance.Effects of an immunosuppressive treatment in the GRMD dog model of Duchenne muscular dystrophy.Facioscapulohumeral muscular dystrophy (FSHD) region gene 1 (FRG1) is a dynamic nuclear and sarcomeric protein.Human embryonic myosin heavy chain cDNA. Interspecies sequence conservation of the myosin rod, chromosomal locus and isoform specific transcription of the gene.Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice.Absence of developmental and unconventional myosin heavy chain in human suprahyoid muscles.Hindlimb skeletal muscle function in myostatin-deficient mice.
P2860
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P2860
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
description
1988 nî lūn-bûn
@nan
1988年の論文
@ja
1988年学术文章
@wuu
1988年学术文章
@zh-cn
1988年学术文章
@zh-hans
1988年学术文章
@zh-my
1988年学术文章
@zh-sg
1988年學術文章
@yue
1988年學術文章
@zh
1988年學術文章
@zh-hant
name
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@en
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@nl
type
label
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@en
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@nl
prefLabel
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@en
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@nl
P2093
P1433
P1476
Fast muscle fibers are preferentially affected in Duchenne muscular dystrophy.
@en
P2093
P304
P356
10.1016/0092-8674(88)90463-1
P407
P577
1988-02-01T00:00:00Z