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. 2014 May 22;6:99. doi: 10.3389/fnagi.2014.00099

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Copyright © 2014 Rudolf, Khan, Labeit and Deschenes.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Scheme depicting the putative life cycle of AChR at the vertebrate NMJ. Upon assembly in the ER and glycosylation in the Golgi apparatus, AChR is delivered by exocytosis to the post-synaptic membrane where it is clustered by means of agrin/MuSK/Lrp4/rapsyn complex, to fulfill its major function, i.e., mediating neuromuscular transmission. Subsequently, AChR is endocytosed and can then be recycled using a cooperative function of myosin Va, PKA type I, and rapsyn, or degraded, presumably via autophagic decay in a MuRF1-dependent manner. Decision-making between recycling or degradation appears to be subject to manifold signals including CaMKII and PKC.