ArticleThe Journal of cell biology1993
A role for the dystrophin-glycoprotein complex as a transmembrane linker between laminin and actin.
Article in The Journal of cell biology, 1993. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 553 papers.
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Who cites it
553 citing papers in PubMed, 1,378 citations in OpenAlex.
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- Alterations of actin in aging.Journal of cell science · 2026Review
- Prime Editing Mediated Generation and Correction of the mdx5cv Mutation Restores Dystrophin Expression in Myoblasts.International journal of molecular sciences · 2026Article
- Duchenne muscular dystrophy: from gene to gene-ius therapies.Skeletal muscle · 2026Review
- Low-dose MyoAAV 2A-mediated delivery of engineered micro-utrophin achieves pan- muscle tissue distribution with elevated muscle function in Duchenne muscular dystrophy.Journal of translational medicine · 2026Article
- 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
- Quantitative tandem mass tag-based serum proteomics for longitudinal biomarker monitoring in Duchenne muscular dystrophy.Clinical proteomics · 2026Article
- The atomic structure of human dystrophin spectrin-like repeat 24.Acta crystallographica. Section F, Structural biology communications · 2026Article
- Gmppb-mutant mice exhibit dystroglycanopathy symptoms that are rescued with GSK3β inhibition or AAV-mediated GMPPB gene replacement.Nature communications · 2026Article
- Generation of a novel Dysferlin microdeletion knock-in mouse model mimicking muscular dystrophy-like pathology.Scientific reports · 2026Article
- PPMO-based exon skipping therapy improves respiratory function in theMolecular therapy. Nucleic acids · 2026Article
- Molecular Insights and Orthopedic Management in Muscular Dystrophies: A Comprehensive Review.International journal of molecular sciences · 2026Review
- Recent advances in the synthesis of α-dystroglycanRSC advances · 2026Review
- Five key challenges for the plasma membrane insertion of nicotinic acetylcholine receptors in cellular model systems.Molecular and cellular biochemistry · 2026Review
- Proteomics-based evaluation of AAV dystrophin gene therapy outcomes in mdx skeletal muscle.JCI insight · 2026Article
- Disease exacerbation in human DMD MYOrganoids enables gene therapy evaluation and unveils persistence of fibrotic activity.NPJ Regenerative medicine · 2026Article
- A unified model for Duchenne muscular dystrophy gene involvement in cancer: context-dependent tumour suppression and oncogenicity.FEBS open bio · 2026Article
- Analysis of Dystrophin-Associated Glycoproteins: Focus on Expression and Glycosylation of Dystroglycan in Skeletal Muscle.Methods in molecular biology (Clifton, N.J.) · 2026Article
- Autosomal Dominant MissenseHuman mutation · 2026Article
493 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
The dystrophin-glycoprotein complex was tested for interaction with several components of the extracellular matrix as well as actin. The 156-kD dystrophin-associated glycoprotein (156-kD dystroglycan) specifically bound laminin in a calcium-dependent manner and was inhibited by NaCl (IC50 = 250 mM) but was not affected by 1,000-fold (wt/wt) excesses of lactose, IKVAV, or YIGSR peptides. Laminin binding was inhibited by heparin (IC50 = 100 micrograms/ml), suggesting that one of the heparin-binding domains of laminin is involved in binding dystroglycan while negatively charged oligosaccharide moieties on dystroglycan were found to be necessary for its laminin-binding activity. No interaction between any component of the dystrophin-glycoprotein complex and fibronectin, collagen I, collagen IV, entactin, or heparan sulfate proteoglycan was detected by 125I-protein overlay and/or extracellular matrix protein-Sepharose precipitation. In addition, laminin-Sepharose quantitatively precipitated purified dystrophin-glycoprotein complex, demonstrating that the laminin-binding site is accessible when dystroglycan is associated with the complex. Dystroglycan of nonmuscle tissues also bound laminin. However, the other proteins of the striated muscle dystrophin-glycoprotein complex appear to be absent, antigenically dissimilar or less tightly associated with dystroglycan in nonmuscle tissues. Finally, we show that the dystrophin-glycoprotein complex cosediments with F-actin but does not bind calcium or calmodulin. Our results support a role for the striated muscle dystrophin-glycoprotein complex in linking the actin-based cytoskeleton with the extracellular matrix. Furthermore, our results suggest that dystrophin and dystroglycan may play substantially different functional roles in nonmuscle tissues.
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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.