ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1998
alpha-Dystroglycan functions in acetylcholine receptor aggregation but is not a coreceptor for agrin-MuSK signaling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 72 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
- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- Extracellular signal-regulated kinases 1 and 2 regulate neuromuscular junction and myofiber phenotypes in mammalian skeletal muscle.Neuroscience letters · 2020Review
- Pathogenic effects of agrin V1727F mutation are isoform specific and decrease its expression and affinity for HSPGs and LRP4.Human molecular genetics · 2019Article
- The roles of dystroglycan in the nervous system: insights from animal models of muscular dystrophy.Disease models & mechanisms · 2018Review
- Novel SEA and LG2 Agrin mutations causing congenital Myasthenic syndrome.Orphanet journal of rare diseases · 2017Article
- Can Human Pluripotent Stem Cell-Derived Cardiomyocytes Advance Understanding of Muscular Dystrophies?Journal of neuromuscular diseases · 2016Review
- Gephyrin clusters are absent from small diameter primary afferent terminals despite the presence of GABA(A) receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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- LG2 agrin mutation causing severe congenital myasthenic syndrome mimics functional characteristics of non-neural (z-) agrin.Human genetics · 2012Article
- Modulation of agrin-induced acetylcholine receptor clustering by extracellular signal-regulated kinases 1 and 2 in cultured myotubes.The Journal of biological chemistry · 2010Article
- The roles of the dystrophin-associated glycoprotein complex at the synapse.Molecular neurobiology · 2010Review
- Muscular dystrophy associated with alpha-dystroglycan deficiency in Sphynx and Devon Rex cats.Neuromuscular disorders : NMD · 2008Article
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- Article
- Neuromyelitis optica pathogenesis and aquaporin 4.Journal of neuroinflammation · 2008Review
- Dp71, utrophin and beta-dystroglycan expression and distribution in PC12/L6 cell cocultures.Neuroreport · 2007Article
- Differential requirement for MuSK and dystroglycan in generating patterns of neuromuscular innervation.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Neuregulin induces the expression of transcription factors and myosin heavy chains typical of muscle spindles in cultured human muscle.Proceedings of the National Academy of Sciences of the United States of America · 2004Article
- The COOH-terminal domain of agrin signals via a synaptic receptor in central nervous system neurons.The Journal of cell biology · 2003Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
alpha-dystroglycan (alpha-DG) is an agrin-binding protein that has been implicated in acetylcholine receptor (AChR) clustering, but it is unclear whether it acts as a coreceptor involved in initial agrin signaling or as a component involved in later events. To investigate its role, we have generated antisense derivatives of the C2 mouse muscle cell line, which have reduced alpha-DG expression. When compared with wild-type cells, the alpha-DG-deficient myotubes have a dramatic reduction in the number of spontaneous and agrin-induced AChR clusters. Several findings suggest that this decrease in AChR clustering is likely not because of a defect in agrin signaling through the MuSK receptor tyrosine kinase. Compared with wild-type cells, the alpha-DG-deficient cell lines showed only a transient reduction in the level of agrin-induced MuSK tyrosine phosphorylation and no reduction in AChR beta-subunit tyrosine phosphorylation. Additionally, agrin-induced phosphorylation of MuSK in wild-type myotubes was not decreased using agrin fragments that lack the domain primarily responsible for binding to alpha-DG. Finally, neural agrin-induced phosphorylation of MuSK was unaffected by treatments such as excess muscle agrin or anti-alpha-DG antibodies, both of which block agrin-alpha-DG binding. Together, these results suggest that alpha-DG is not required for agrin-MuSK signaling but rather that it may play a role elsewhere in the clustering pathway, such as in the downstream consolidation or maintenance of AChR clusters.
Indexed as
Identifiers
9698325PMC6793207W1921001017What OpenQuestion holds
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.