Enhanced expression of the alpha 7 beta 1 integrin reduces muscular dystrophy and restores viability in dystrophic mice
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The potential of sarcospan in adhesion complex replacement therapeutics for the treatment of muscular dystrophyDistinct roles for laminin globular domains in laminin alpha1 chain mediated rescue of murine laminin alpha2 chain deficiencyAnimal models of Duchenne muscular dystrophy: from basic mechanisms to gene therapyAbsence of alpha 7 integrin in dystrophin-deficient mice causes a myopathy similar to Duchenne muscular dystrophyCytoplasmic gamma-actin expression in diverse animal models of muscular dystrophyModulation of alpha7-integrin-mediated adhesion and expression by platelet-derived growth factor in vascular smooth muscle cellsThe amphoterin (HMGB1)/receptor for advanced glycation end products (RAGE) pair modulates myoblast proliferation, apoptosis, adhesiveness, migration, and invasiveness. Functional inactivation of RAGE in L6 myoblasts results in tumor formation in vivGenetically determined proteolytic cleavage modulates alpha7beta1 integrin function.Laminin alpha1 chain mediated reduction of laminin alpha2 chain deficient muscular dystrophy involves integrin alpha7beta1 and dystroglycan.Skeletal muscle-specific ablation of gamma(cyto)-actin does not exacerbate the mdx phenotype.Dystrophin glycoprotein complex-associated Gbetagamma subunits activate phosphatidylinositol-3-kinase/Akt signaling in skeletal muscle in a laminin-dependent manner.Genome Editing and Muscle Stem Cells as a Therapeutic Tool for Muscular Dystrophies.Emerging genetic therapies to treat Duchenne muscular dystrophySubstrate and strain alter the muscle-derived mesenchymal stem cell secretome to promote myogenesis.Overexpression of the cytotoxic T cell GalNAc transferase in skeletal muscle inhibits muscular dystrophy in mdx miceA human-specific deletion in mouse Cmah increases disease severity in the mdx model of Duchenne muscular dystrophySarcospan-dependent Akt activation is required for utrophin expression and muscle regeneration.Soleus muscle in glycosylation-deficient muscular dystrophy is protected from contraction-induced injurySarcospan integration into laminin-binding adhesion complexes that ameliorate muscular dystrophy requires utrophin and α7 integrin.Experimental models of duchenne muscular dystrophy: relationship with cardiovascular disease.Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice.Transgenic expression of Laminin α1 chain does not prevent muscle disease in the mdx mouse model for Duchenne muscular dystrophy.Therapeutic approaches to muscular dystrophy.Duchenne muscular dystrophy gene therapy: Lost in translation?Dystrophin-glycoprotein complex: post-translational processing and dystroglycan function.Transgenic overexpression of dystroglycan does not inhibit muscular dystrophy in mdx miceTransgenic expression of {alpha}7{beta}1 integrin maintains muscle integrity, increases regenerative capacity, promotes hypertrophy, and reduces cardiomyopathy in dystrophic mice.A role for Galgt1 in skeletal muscle regeneration.TAT-μUtrophin mitigates the pathophysiology of dystrophin and utrophin double-knockout mice.Sarcolemma instability during mechanical activity in Largemyd cardiac myocytes with loss of dystroglycan extracellular matrix receptor functionIntegrin-dependent pathologies.Gamma-sarcoglycan is required for the response of archvillin to mechanical stimulation in skeletal muscle.Expression of the dystrophin isoform Dp116 preserves functional muscle mass and extends lifespan without preventing dystrophy in severely dystrophic miceSERCA1 overexpression minimizes skeletal muscle damage in dystrophic mouse models.ADAM12 alleviates the skeletal muscle pathology in mdx dystrophic mice.Alpha7beta1 integrin does not alleviate disease in a mouse model of limb girdle muscular dystrophy type 2Fβ1D chain increases α7β1 integrin and laminin and protects against sarcolemmal damage in mdx miceViral-mediated gene therapy for the muscular dystrophies: successes, limitations and recent advancesSarcoglycan complex in masseter and sternocleidomastoid muscles of baboons: an immunohistochemical study.Postnatal overexpression of the CT GalNAc transferase inhibits muscular dystrophy in mdx mice without altering muscle growth or neuromuscular development: evidence for a utrophin-independent mechanism
P2860
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P2860
Enhanced expression of the alpha 7 beta 1 integrin reduces muscular dystrophy and restores viability in dystrophic mice
description
2001 nî lūn-bûn
@nan
2001年の論文
@ja
2001年学术文章
@wuu
2001年学术文章
@zh-cn
2001年学术文章
@zh-hans
2001年学术文章
@zh-my
2001年学术文章
@zh-sg
2001年學術文章
@yue
2001年學術文章
@zh
2001年學術文章
@zh-hant
name
Enhanced expression of the alp ...... s viability in dystrophic mice
@ast
Enhanced expression of the alp ...... s viability in dystrophic mice
@en
type
label
Enhanced expression of the alp ...... s viability in dystrophic mice
@ast
Enhanced expression of the alp ...... s viability in dystrophic mice
@en
prefLabel
Enhanced expression of the alp ...... s viability in dystrophic mice
@ast
Enhanced expression of the alp ...... s viability in dystrophic mice
@en
P2093
P2860
P356
P1476
Enhanced expression of the alp ...... s viability in dystrophic mice
@en
P2093
D J Kaufman
G Q Wallace
S J Kaufman
P2860
P304
P356
10.1083/JCB.152.6.1207
P407
P50
P577
2001-03-01T00:00:00Z