ArticleJournal of neuropathology and experimental neurology2011
Dysferlin, annexin A1, and mitsugumin 53 are upregulated in muscular dystrophy and localize to longitudinal tubules of the T-system with stretch.
Article in Journal of neuropathology and experimental neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
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Who cites it
61 citing papers in PubMed, 108 citations in OpenAlex.
- Accumulation of membrane repair-associated proteins and mature myostatin are novel markers of muscle pathophysiology in Pompe disease.Acta neuropathologica communications · 2026Article
- MG53, a Regenerative Myokine Linking Skeletal Muscle to Cardiac Repair.Biomolecules · 2026Review
- A Novel Dysferlin-Binding Kinase CK2α Promotes Plasma Membrane Repair in Dysferlinopathy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026Article
- Dysferlin and the Regulation of CaCells · 2025Review
- The Dysferlinopathies Conundrum: Clinical Spectra, Disease Mechanism and Genetic Approaches for Treatments.Biomolecules · 2024Review
- Wound Repair of the Cell Membrane: Lessons fromCells · 2024Review
- Minimal expression of dysferlin prevents development of dysferlinopathy in dysferlin exon 40a knockout mice.Acta neuropathologica communications · 2023Article
- Dynamics of Actin Cytoskeleton and Their Signaling Pathways during Cellular Wound Repair.Cells · 2022Article
- Activation of SIRT1 promotes membrane resealing via cortactin.Scientific reports · 2022Article
- Evidence of an Annexin A4 mediated plasma membrane repair response to biomechanical strain associated with glaucoma pathogenesis.Journal of cellular physiology · 2022Article
- Article
- Cytoplasmic HDAC4 regulates the membrane repair mechanism in Duchenne muscular dystrophy.Journal of cachexia, sarcopenia and muscle · 2022Article
- The C2 domains of dysferlin: roles in membrane localization, CaThe Journal of physiology · 2022Article
- Loss of dysferlin or myoferlin results in differential defects in excitation-contraction coupling in mouse skeletal muscle.Scientific reports · 2021Article
- Muscle multiorgan crosstalk with MG53 as a myokine for tissue repair and regeneration.Current opinion in pharmacology · 2021Review
- Annexins and Membrane Repair Dysfunctions in Muscular Dystrophies.International journal of molecular sciences · 2021Review
- Article
- Exosome-mediated improvement in membrane integrity and muscle function in dystrophic mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Very Low Residual Dystrophin Quantity Is Associated with Milder Dystrophinopathy.Annals of neurology · 2021Article
- Review
1 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
16 authors at 1 institution in 1 country.
Funding
Abstract
Mutations in dysferlin cause an inherited muscular dystrophy because of defective membrane repair. Three interacting partners of dysferlin are also implicated in membrane resealing: caveolin-3 (in limb girdle muscular dystrophy type 1C), annexin A1, and the newly identified protein mitsugumin 53 (MG53). Mitsugumin 53 accumulates at sites of membrane damage, and MG53-knockout mice display a progressive muscular dystrophy. This study explored the expression and localization of MG53 in human skeletal muscle, how membrane repair proteins are modulated in various forms of muscular dystrophy, and whether MG53 is a primary cause of human muscle disease. Mitsugumin 53 showed variable sarcolemmal and/or cytoplasmic immunolabeling in control human muscle and elevated levels in dystrophic patients. No pathogenic MG53 mutations were identified in 50 muscular dystrophy patients, suggesting that MG53 is unlikely to be a common cause of muscular dystrophy in Australia. Western blot analysis confirmed upregulation of MG53, as well as of dysferlin, annexin A1, and caveolin-3 to different degrees, in different muscular dystrophies. Importantly, MG53, annexin A1, and dysferlin localize to the t-tubule network and show enriched labeling at longitudinal tubules of the t-system in overstretch. Our results suggest that longitudinal tubules of the t-system may represent sites of physiological membrane damage targeted by this membrane repair complex.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.