Title : The function of cortactin in the clustering of acetylcholine receptors at the vertebrate neuromuscular junction.

Pub. Date : 2009 Dec 29

PMID : 20041195






4 Functional Relationships(s)
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1 BACKGROUND: Postsynaptic enrichment of acetylcholine receptors (AChRs) at the vertebrate neuromuscular junction (NMJ) depends on the activation of the muscle receptor tyrosine MuSK by neural agrin. Tyrosine agrin Homo sapiens
2 Cortactin was further preferentially tyrosine phosphorylated at AChR clustering sites and treatment of myotubes with agrin significantly enhanced the tyrosine phosphorylation of cortactin. Tyrosine agrin Homo sapiens
3 Cortactin was further preferentially tyrosine phosphorylated at AChR clustering sites and treatment of myotubes with agrin significantly enhanced the tyrosine phosphorylation of cortactin. Tyrosine agrin Homo sapiens
4 Importantly, forced expression in myotubes of a tyrosine phosphorylation-defective cortactin mutant (but not wild-type cortactin) suppressed agrin-dependent AChR clustering, as did the reduction of endogenous cortactin levels using RNA interference, and introduction of the mutant cortactin into muscle cells potently inhibited synaptic AChR aggregation in response to innervation. Tyrosine agrin Homo sapiens