||An important event in the formation of neuromuscular junction (NMJ) is the aggregation of acetylcholine receptors (AChRs) in muscle juxtaposed to the presynaptic nerve terminal. Neural agrin, a component of the synaptic basal lamina, induces AChR clustering via the activation of a receptor tyrosine kinase, muscle-specific kinase (MuSK). Recently, components of the Wnt signaling pathway, such as Dishevelled (Dsh) and Adenomatous polyposis coli (APC), have been implicated in the regulation of AChR clustering. Axis inhibitor (Axin), an interacting partner of both Dsh and APC, has previously been identified as a scaffold protein critical for the degradation of beta-catenin in Wnt signaling. To explore if Axin may also play a role in NMJ formation, we first examined the expression of Axin in cultured C2C12 cells and rat skeletal muscle during development. We found that Axin protein expression could be detected in C2C12 myoblasts and differentiated myotubes. In addition, Northern blot analysis showed that while Axin transcript could be prominently detected in rat skeletal muscle at embryonic day 18, its expression level decreased during postnatal stages. Interestingly, induction of Axin transcript was observed in muscle following denervation. Furthermore, preliminary result from knockdown and overexpression studies revealed that Axin might negatively regulate the formation of AChR clusters. Taken together, our findings suggest that in addition to Dsh and APC, Axin may also play a role in the regulation of NMJ formation/maintenance.