Muscle genome-wide expression profiling during disease evolution in mdx mice.
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Differential Gene Expression Profiling of Dystrophic Dog Muscle after MuStem Cell TransplantationEvaluation of skeletal and cardiac muscle function after chronic administration of thymosin beta-4 in the dystrophin deficient mouse.Drosophila melanogaster muscle LIM protein and alpha-actinin function together to stabilize muscle cytoarchitecture: a potential role for Mlp84B in actin-crosslinking.A dual acting compound releasing nitric oxide (NO) and ibuprofen, NCX 320, shows significant therapeutic effects in a mouse model of muscular dystrophy.Influences of desmin and keratin 19 on passive biomechanical properties of mouse skeletal muscle.Deletion of periostin reduces muscular dystrophy and fibrosis in mice by modulating the transforming growth factor-β pathway.Multi-level omics analysis in a murine model of dystrophin loss and therapeutic restoration.Cathepsin S Contributes to the Pathogenesis of Muscular Dystrophy in Mice.Wnt protein-mediated satellite cell conversion in adult and aged mice following voluntary wheel running.Quantitative proteome profiling of dystrophic dog skeletal muscle reveals a stabilized muscular architecture and protection against oxidative stress after systemic delivery of MuStem cells.Lack of dystrophin in mdx mice modulates the expression of genes involved in neuron survival and differentiation.Pathoproteomic profiling of the skeletal muscle matrisome in dystrophinopathy associated myofibrosis.Tumor Necrosis Factor Alpha and Insulin-Like Growth Factor 1 Induced Modifications of the Gene Expression Kinetics of Differentiating Skeletal Muscle Cells.Periostin as a multifunctional modulator of the wound healing response.Actin filaments-A target for redox regulationLabel-free mass spectrometric analysis of the mdx-4cv diaphragm identifies the matricellular protein periostin as a potential factor involved in dystrophinopathy-related fibrosis.Comparative transcriptome analysis of muscular dystrophy models Large(myd), Dmd(mdx)/Large(myd) and Dmd(mdx): what makes them different?Mesoangioblasts suppress T cell proliferation through IDO and PGE-2-dependent pathways.Reducing sarcolipin expression mitigates Duchenne muscular dystrophy and associated cardiomyopathy in mice.Proteomic assessment of the acute phase of dystrophin deficiency in mdx mice.Increased sarcolipin expression and decreased sarco(endo)plasmic reticulum Ca2+ uptake in skeletal muscles of mouse models of Duchenne muscular dystrophy.Transcriptomic signature to oxidative stress exposure at the time of embryonic genome activation in bovine blastocysts.Glucocorticoids Improve Myogenic Differentiation In Vitro by Suppressing the Synthesis of Versican, a Transitional Matrix Protein Overexpressed in Dystrophic Skeletal Muscles.The MICALs are a Family of F-actin Dismantling Oxidoreductases Conserved from Drosophila to Humans.
P2860
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P2860
Muscle genome-wide expression profiling during disease evolution in mdx mice.
description
2009 nî lūn-bûn
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2009年の論文
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2009年学术文章
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2009年学术文章
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2009年学术文章
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2009年学术文章
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2009年学术文章
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2009年學術文章
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2009年學術文章
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2009年學術文章
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name
Muscle genome-wide expression profiling during disease evolution in mdx mice.
@en
Muscle genome-wide expression profiling during disease evolution in mdx mice.
@nl
type
label
Muscle genome-wide expression profiling during disease evolution in mdx mice.
@en
Muscle genome-wide expression profiling during disease evolution in mdx mice.
@nl
prefLabel
Muscle genome-wide expression profiling during disease evolution in mdx mice.
@en
Muscle genome-wide expression profiling during disease evolution in mdx mice.
@nl
P2093
P2860
P1476
Muscle genome-wide expression profiling during disease evolution in mdx mice
@en
P2093
Claudia Ruiz-Roig
Fatima Nuñez
Francina Munell
Manuel Roig-Quilis
Mario Marotta
Yaris Sarria
P2860
P304
P356
10.1152/PHYSIOLGENOMICS.90370.2008
P577
2009-02-17T00:00:00Z