ArticleThe Journal of cell biology1997
Laminin-induced acetylcholine receptor clustering: an alternative pathway.
Article in The Journal of cell biology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
38 citing papers in PubMed, 136 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
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- The role of the dystrophin glycoprotein complex on the neuromuscular system.Neuroscience letters · 2020Review
- An improved method for culturing myotubes on laminins for the robust clustering of postsynaptic machinery.Scientific reports · 2020Article
- Enzymatically crosslinked gelatin-laminin hydrogels for applications in neuromuscular tissue engineering.Biomaterials science · 2020Article
- The Neuromuscular Junction in Health and Disease: Molecular Mechanisms Governing Synaptic Formation and Homeostasis.Frontiers in molecular neuroscience · 2020Review
- The Effect of Laminin-111 Hydrogels on Muscle Regeneration in a Murine Model of Injury.Tissue engineering. Part A · 2019Article
- Regulation of Myogenic Activity by Substrate and Electrical StimulationBioResearch open access · 2019Article
- Sodium nitrate decreases agrin-induced acetylcholine receptor clustering.BMC pharmacology & toxicology · 2016Article
- Acetylcholine receptor (AChR) clustering is regulated both by glycogen synthase kinase 3β (GSK3β)-dependent phosphorylation and the level of CLIP-associated protein 2 (CLASP2) mediating the capture of microtubule plus-ends.The Journal of biological chemistry · 2014Article
- Muscle-specific kinase (MuSK) autoantibodies suppress the MuSK pathway and ACh receptor retention at the mouse neuromuscular junction.The Journal of physiology · 2014Article
- Skeletal muscle IP3R1 receptors amplify physiological and pathological synaptic calcium signals.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Aberrant development of neuromuscular junctions in glycosylation-defective Large(myd) mice.Neuromuscular disorders : NMD · 2009Article
- Article
- Laminins promote postsynaptic maturation by an autocrine mechanism at the neuromuscular junction.The Journal of cell biology · 2008Article
- Cell culture-based analysis of postsynaptic membrane assembly in muscle cells.Biological procedures online · 2008Article
- Induction of myasthenia by immunization against muscle-specific kinase.The Journal of clinical investigation · 2006Article
- MuSK signaling at the neuromuscular junction.Journal of molecular neuroscience : MN · 2006Article
- Beta1 integrins in muscle, but not in motor neurons, are required for skeletal muscle innervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Nerve-independent formation of a topologically complex postsynaptic apparatus.The Journal of cell biology · 2004Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The induction of acetylcholine receptor (AChR) clustering by neurally released agrin is a critical, early step in the formation of the neuromuscular junction. Laminin, a component of the muscle fiber basal lamina, also induces AChR clustering. We find that induction of AChR clustering in C2 myotubes is specific for laminin-1; neither laminin-2 (merosin) nor laminin-11 (a synapse-specific isoform) are active. Moreover, laminin-1 induces AChR clustering by a pathway that is independent of that used by neural agrin. The effects of laminin-1 and agrin are strictly additive and occur with different time courses. Most importantly, laminin- 1-induced clustering does not require MuSK, a receptor tyrosine kinase that is part of the receptor complex for agrin. Laminin-1 does not cause tyrosine phosphorylation of MuSK in C2 myotubes and induces AChR clustering in myotubes from MuSK-/- mice that do not respond to agrin. In contrast to agrin, laminin-1 also does not induce tyrosine phosphorylation of the AChR, demonstrating that AChR tyrosine phosphorylation is not required for clustering in myotubes. Laminin-1 thus acts by a mechanism that is independent of that used by agrin and may provide a supplemental pathway for AChR clustering during synaptogenesis.
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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.