ArticleThe Journal of cell biology1995
Immobilization of nicotinic acetylcholine receptors in mouse C2 myotubes by agrin-induced protein tyrosine phosphorylation.
Article in The Journal of cell biology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 67 citations in OpenAlex.
- Exploring Missense Mutations in Tyrosine Kinases Implicated with Neurodegeneration.Molecular neurobiology · 2017Review
- Control of rapsyn stability by the CUL-3-containing E3 ligase complex.The Journal of biological chemistry · 2009Article
- Rapsyn carboxyl terminal domains mediate muscle specific kinase-induced phosphorylation of the muscle acetylcholine receptor.Neuroscience · 2008Article
- Tyrosine phosphatases such as SHP-2 act in a balance with Src-family kinases in stabilization of postsynaptic clusters of acetylcholine receptors.BMC neuroscience · 2007Article
- Alpha7 neuronal nicotinic acetylcholine receptors are negatively regulated by tyrosine phosphorylation and Src-family kinases.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2005Article
- Clustering of nicotinic acetylcholine receptors: from the neuromuscular junction to interneuronal synapses.Molecular neurobiology · 2002Review
- Src-class kinases act within the agrin/MuSK pathway to regulate acetylcholine receptor phosphorylation, cytoskeletal anchoring, and clustering.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
- Agrin-induced phosphorylation of the acetylcholine receptor regulates cytoskeletal anchoring and clustering.The Journal of cell biology · 2001Article
- The myristoylated protein rapsyn is cotargeted with the nicotinic acetylcholine receptor to the postsynaptic membrane via the exocytic pathway.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2000Article
- Roles of rapsyn and agrin in interaction of postsynaptic proteins with acetylcholine receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1999Article
- Processing of ARIA and release from isolated nerve terminals.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 1999Review
- alpha-Dystroglycan functions in acetylcholine receptor aggregation but is not a coreceptor for agrin-MuSK signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- A role of tyrosine phosphatase in acetylcholine receptor cluster dispersal and formation.The Journal of cell biology · 1998Article
- Intracellular calcium regulates agrin-induced acetylcholine receptor clustering.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1998Article
- Laminin-induced acetylcholine receptor clustering: an alternative pathway.The Journal of cell biology · 1997Article
- Neural agrin induces ectopic postsynaptic specializations in innervated muscle fibers.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
- Association of muscle-specific kinase MuSK with the acetylcholine receptor in mammalian muscle.The EMBO journal · 1997Article
- Intercellular communication that mediates formation of the neuromuscular junction.Molecular neurobiology · 1997Review
- AChR phosphorylation and aggregation induced by an agrin fragment that lacks the binding domain for alpha-dystroglycan.The EMBO journal · 1996Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Agrin induces the formation of highly localized specializations on myotubes at which nicotinic acetylcholine receptors (AChRs) and many other components of the postsynaptic apparatus at the vertebrate skeletal neuromuscular junction accumulate. Agrin also induces AChR tyrosine phosphorylation. Treatments that inhibit tyrosine phosphorylation prevent AChR aggregation. To examine further the relationship between tyrosine phosphorylation and receptor aggregation, we have used the technique of fluorescence recovery after photobleaching to assess the lateral mobility of AChRs and other surface proteins in mouse C2 myotubes treated with agrin or with pervanadate, a protein tyrosine phosphatase inhibitor. Agrin induced the formation of patches in C2 myotubes that stained intensely with anti-phosphotyrosine antibodies and within which AChRs were relatively immobile. Pervanadate, on the other hand, increased protein tyrosine phosphorylation throughout the myotube and caused a reduction in the mobility of diffusely distributed AChRs, without affecting the mobility of other membrane proteins. Pervanadate, like agrin, caused an increase in AChR tyrosine phosphorylation and a decrease in the rate at which AChRs could be extracted from intact myotubes by mild detergent treatment, suggesting that immobilized receptors were phosphorylated and therefore less extractable. Indeed, phosphorylated receptors were extracted from agrin-treated myotubes more slowly than nonphosphorylated receptors. AChR aggregates at developing neuromuscular junctions in embryonic rat muscles also labeled with anti-phosphotyrosine antibodies, suggesting that tyrosine phosphorylation could mediate AChR aggregation in vivo as well. Thus, agrin appears to induce AChR aggregation by creating circumscribed domains of increased protein tyrosine phosphorylation within which receptors become phosphorylated and immobilized.
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