ArticleThe Journal of cell biology1991
Dystrophin-associated proteins are greatly reduced in skeletal muscle from mdx mice.
Article in The Journal of cell biology, 1991. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 426 citations in OpenAlex.
- Cytoplasmic region of beta-dystroglycan is essential for postsynaptic maturation and neuromuscular function in mice.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Manual Immunofluorescence Staining for Dystrophin and Key Dystrophin-Associated Proteins.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Quantitative 3D assessment of muscle dystrophy through X-ray phase-contrast tomography.Scientific reports · 2025Article
- Improvement of Spontaneous Locomotor Activity in a Murine Model of Duchenne Muscular Dystrophy by N-Acetylglucosamine Alone and in Combination With Prednisolone.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Altered acute metabolic response to muscle stimulation in muscular dystrophic mice observed by phosphorus-31 magnetic resonance spectroscopy and fingerprinting.Journal of applied physiology (Bethesda, Md. : 1985) · 2025Article
- Muscle stem cells in Duchenne muscular dystrophy exhibit molecular impairments and altered cell fate trajectories impacting regenerative capacity.Cell death & disease · 2025Article
- Why is early-onset atrial fibrillation uncommon in patients with Duchenne muscular dystrophy? Insights from the mdx mouse.Cardiovascular research · 2024Article
- How Can Proteomics Help to Elucidate the Pathophysiological Crosstalk in Muscular Dystrophy and Associated Multi-System Dysfunction?Proteomes · 2024Article
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Multi-omics analysis of sarcospan overexpression in mdx skeletal muscle reveals compensatory remodeling of cytoskeleton-matrix interactions that promote mechanotransduction pathways.Skeletal muscle · 2023Article
- Verification of Protein Changes Determined by 2D-DIGE Based Proteomics Using Immunofluorescence Microscopy.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Histological and Histochemical Microscopy Used to Verify 2D-DIGE Pathoproteomics.Methods in molecular biology (Clifton, N.J.) · 2023Article
- Proteomic Identification of Markers of Membrane Repair, Regeneration and Fibrosis in the Aged and Dystrophic Diaphragm.Life (Basel, Switzerland) · 2022Article
- Optimized lentiviral vector to restore full-length dystrophin via a cell-mediated approach in a mouse model of Duchenne muscular dystrophy.Molecular therapy. Methods & clinical development · 2022Article
- Histopathology of Duchenne muscular dystrophy in correlation with changes in proteomic biomarkers.Histology and histopathology · 2022Review
- Alteration of skeletal and cardiac muscles function inIntractable & rare diseases research · 2021Article
- Contraction-Induced Loss of Plasmalemmal Electrophysiological Function Is Dependent on the Dystrophin Glycoprotein Complex.Frontiers in physiology · 2021Article
- Genome Editing-Mediated Utrophin Upregulation in Duchenne Muscular Dystrophy Stem Cells.Molecular therapy. Nucleic acids · 2020Article
- Mutation-independent Proteomic Signatures of Pathological Progression in Murine Models of Duchenne Muscular Dystrophy.Molecular & cellular proteomics : MCP · 2020Article
- The Effect of Deflazacort Treatment on the Functioning of Skeletal Muscle Mitochondria in Duchenne Muscular Dystrophy.International journal of molecular sciences · 2020Article
79 more citing papers are in PubMed but not listed here.
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dystrophin, the protein product of the human Duchenne muscular dystrophy gene, exists in skeletal muscle as a large oligomeric complex that contains four glycoproteins of 156, 50, 43, and 35 kD and a protein of 59 kD. Here, we investigated the relative abundance of each of the components of the dystrophin-glycoprotein complex in skeletal muscle from normal and mdx mice, which are missing dystrophin. Immunoblot analysis using total muscle membranes from control and mdx mice of ages 1 d to 30 wk found that all of the dystrophin-associated proteins were greatly reduced (80-90%) in mdx mouse skeletal muscle. The specificity of the loss of the dystrophin-associated glycoproteins was demonstrated by the finding that the major glycoprotein composition of skeletal muscle membranes from normal and mdx mice was identical. Furthermore, skeletal muscle membranes from the dystrophic dy/dy mouse exhibited a normal density of dystrophin and dystrophin-associated proteins. Immunofluorescence microscopy confirmed the results from the immunoblot analysis and showed a drastically reduced density of dystrophin-associated proteins in mdx muscle cryosections compared with normal and dy/dy mouse muscle. Therefore, our results demonstrate that all of the dystrophin-associated proteins are significantly reduced in mdx skeletal muscle and suggest that the loss of dystrophin-associated proteins is due to the absence of dystrophin and not due to secondary effects of muscle fiber degradation.
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