Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice.
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The potential of sarcospan in adhesion complex replacement therapeutics for the treatment of muscular dystrophyThe Dystrophin Complex: Structure, Function, and Implications for TherapyMicroRNA-486-dependent modulation of DOCK3/PTEN/AKT signaling pathways improves muscular dystrophy-associated symptomsLong-term administration of the TNF blocking drug Remicade (cV1q) to mdx mice reduces skeletal and cardiac muscle fibrosis, but negatively impacts cardiac functionSarcospan-dependent Akt activation is required for utrophin expression and muscle regeneration.Sarcospan integration into laminin-binding adhesion complexes that ameliorate muscular dystrophy requires utrophin and α7 integrin.Matrix metalloproteinase-9 inhibition improves proliferation and engraftment of myogenic cells in dystrophic muscle of mdx miceMolecular and cellular mechanisms of skeletal muscle atrophy: an update.RNA-seq and metabolomic analyses of Akt1-mediated muscle growth reveals regulation of regenerative pathways and changes in the muscle secretome.Dystrophin and utrophin expression require sarcospan: loss of α7 integrin exacerbates a newly discovered muscle phenotype in sarcospan-null mice.Inhibition of muscle fibrosis results in increases in both utrophin levels and the number of revertant myofibers in Duchenne muscular dystrophy.Sarcospan: a small protein with large potential for Duchenne muscular dystrophyFour-week rapamycin treatment improves muscular dystrophy in a fukutin-deficient mouse model of dystroglycanopathyDistinct roles of TRAF6 at early and late stages of muscle pathology in the mdx model of Duchenne muscular dystrophy."Get the Balance Right": Pathological Significance of Autophagy Perturbation in Neuromuscular DisordersAxonal pathology in Krabbe's disease: The cytoskeleton as an emerging therapeutic target.ABC of multifaceted dystrophin glycoprotein complex (DGC).Chondroitin sulfate is a crucial determinant for skeletal muscle development/regeneration and improvement of muscular dystrophies.Activation of p38 signaling increases utrophin A expression in skeletal muscle via the RNA-binding protein KSRP and inhibition of AU-rich element-mediated mRNA decay: implications for novel DMD therapeutics.Repression of phosphatidylinositol transfer protein α ameliorates the pathology of Duchenne muscular dystrophy.Autologous serum supplement favours in vitro regenerative paracrine factors synthesis.Muscle-specific microRNA-206 targets multiple components in dystrophic skeletal muscle representing beneficial adaptations.
P2860
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P2860
Myogenic Akt signaling attenuates muscular degeneration, promotes myofiber regeneration and improves muscle function in dystrophin-deficient mdx mice.
description
2011 nî lūn-bûn
@nan
2011 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2011 թվականի հունվարին հրատարակված գիտական հոդված
@hy
2011年の論文
@ja
2011年論文
@yue
2011年論文
@zh-hant
2011年論文
@zh-hk
2011年論文
@zh-mo
2011年論文
@zh-tw
2011年论文
@wuu
name
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@ast
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@en
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@nl
type
label
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@ast
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@en
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@nl
prefLabel
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@ast
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@en
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@nl
P2093
P2860
P356
P1476
Myogenic Akt signaling attenua ...... dystrophin-deficient mdx mice.
@en
P2093
Alan D Grinnell
Bo Ming Chen
Danielle I Kay
Kenneth Walsh
Leonel Martinez
Melissa J Spencer
Michelle H Kim
Rachelle H Crosbie
Renuka T Rudra
P2860
P304
P356
10.1093/HMG/DDR015
P577
2011-01-18T00:00:00Z