Forced expression of dystrophin deletion constructs reveals structure-function correlations.
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Association of the leukocyte plasma membrane with the actin cytoskeleton through coiled coil-mediated trimeric coronin 1 molecules.Dystrobrevin and dystrophin: an interaction through coiled-coil motifsZZ domain of dystrophin and utrophin: topology and mapping of a beta-dystroglycan interaction siteMolecular organization of sarcoglycan complex in mouse myotubes in cultureRecent advances in innovative therapeutic approaches for Duchenne muscular dystrophy: from discovery to clinical trialsMarginal level dystrophin expression improves clinical outcome in a strain of dystrophin/utrophin double knockout miceInteractions between beta 2-syntrophin and a family of microtubule-associated serine/threonine kinasesThe WW domain of dystrophin requires EF-hands region to interact with beta-dystroglycanAssociation of neuronal nitric oxide synthase (nNOS) with alpha1-syntrophin at the sarcolemmaChanges in mechanosensitive channel gating following mechanical stimulation in skeletal muscle myotubes from the mdx mouseIdentification of new dystroglycan complexes in skeletal muscleDifferential association of syntrophin pairs with the dystrophin complexCardiac involvement in patients with muscular dystrophies: magnetic resonance imaging phenotype and genotypic considerations.Dynamic restoration of dystrophin to dystrophin-deficient myotubes.The polyproline site in hinge 2 influences the functional capacity of truncated dystrophins.Dystrophin delivery to muscles of mdx mice using lentiviral vectors leads to myogenic progenitor targeting and stable gene expression.Heart transplantation in patients with dystrophinopathic cardiomyopathy: Review of the literature and personal series.Gene and cell-mediated therapies for muscular dystrophy.Dystrophin and utrophin: genetic analyses of their role in skeletal muscle.Dystrophins, utrophins, and associated scaffolding complexes: role in mammalian brain and implications for therapeutic strategies.The ZZ domain of dystrophin in DMD: making sense of missense mutations.Dystrophin deficiency markedly increases enterovirus-induced cardiomyopathy: a genetic predisposition to viral heart disease.Functional correction of adult mdx mouse muscle using gutted adenoviral vectors expressing full-length dystrophin.Systemic delivery of genes to striated muscles using adeno-associated viral vectors.Gene therapy of mdx mice with large truncated dystrophins generated by recombination using rAAV6.Transduction of skeletal muscles with common reporter genes can promote muscle fiber degeneration and inflammationOur trails and trials in the subsarcolemmal cytoskeleton network and muscular dystrophy researches in the dystrophin era.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.Cytoplasmic gamma-actin contributes to a compensatory remodeling response in dystrophin-deficient muscleTherapeutic approaches to muscular dystrophy.miR-206 represses hypertrophy of myogenic cells but not muscle fibers via inhibition of HDAC4Current status of pharmaceutical and genetic therapeutic approaches to treat DMD.Mechanical and non-mechanical functions of Dystrophin can prevent cardiac abnormalities in Drosophila.Expression of the dystrophin isoform Dp116 preserves functional muscle mass and extends lifespan without preventing dystrophy in severely dystrophic miceAdeno-associated virus vector carrying human minidystrophin genes effectively ameliorates muscular dystrophy in mdx mouse model.Viral-mediated gene therapy for the muscular dystrophies: successes, limitations and recent advancesFollistatin-mediated skeletal muscle hypertrophy is regulated by Smad3 and mTOR independently of myostatinThe dystrophin-associated glycoprotein complex: what parts can you do without?Successful regional delivery and long-term expression of a dystrophin gene in canine muscular dystrophy: a preclinical model for human therapies.Transgenic mdx mice expressing dystrophin with a deletion in the actin-binding domain display a "mild Becker" phenotype.
P2860
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P2860
Forced expression of dystrophin deletion constructs reveals structure-function correlations.
description
1996 nî lūn-bûn
@nan
1996年の論文
@ja
1996年論文
@yue
1996年論文
@zh-hant
1996年論文
@zh-hk
1996年論文
@zh-mo
1996年論文
@zh-tw
1996年论文
@wuu
1996年论文
@zh
1996年论文
@zh-cn
name
Forced expression of dystrophi ...... ructure-function correlations.
@ast
Forced expression of dystrophi ...... ructure-function correlations.
@en
type
label
Forced expression of dystrophi ...... ructure-function correlations.
@ast
Forced expression of dystrophi ...... ructure-function correlations.
@en
prefLabel
Forced expression of dystrophi ...... ructure-function correlations.
@ast
Forced expression of dystrophi ...... ructure-function correlations.
@en
P2093
P2860
P356
P1476
Forced expression of dystrophi ...... tructure-function correlations
@en
P2093
P2860
P304
P356
10.1083/JCB.134.1.93
P407
P577
1996-07-01T00:00:00Z