Phosphoinositide 3-kinase acts through RAC and Cdc42 during agrin-induced acetylcholine receptor clustering.

作者: Viktoria Nizhynska , Ralph Neumueller , Ruth Herbst

DOI: 10.1002/DNEU.20371

关键词:

摘要: The formation of the neuromuscular junction (NMJ) is regulated by nerve-derived heparan sulfate proteoglycan agrin and muscle-specific kinase MuSK. Agrin induces a signal transduction pathway via MuSK, which promotes reorganization postsynaptic muscle membrane. Activation MuSK leads to phosphorylation redistribution acetylcholine receptors (AChRs) other proteins synaptic sites. accumulation high densities AChRs at regions represents hallmark NMJ required for proper function. Here we show that phosphoinositide 3-kinase (PI3-K) component agrin/MuSK signaling pathway. Muscle cells treated with specific PI3-K inhibitors are unable form full-size AChR clusters in response reduced. Moreover, agrin-induced activation Rac Cdc42 impaired presence inhibitors. localized membrane consistent role during signaling. These results put downstream as regulator clustering. Its agrin-stimulated suggests critical function cytoskeletal reorganizations, lead actin-anchored AChRs. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007.

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