Figure 10.

Proposed model of MT/HDAC6/paxillin axis at the NMJ. HDAC6 inhibitors such as TubA and overexpression of paxillin induce a decrease in HDAC6 activity that leads to a hyperacetylation of tubulin. This tubulin hyperacetylation plays a role in the clustering and stability of AChRs at the NMJ. While paxillin colocalizes perfectly with AChRs, HDAC6 is enriched but only partially accumulates at the NMJ. We propose that at the NMJ, HDAC6 is specifically inhibited at sites of AChR incorporation by its endogenous inhibitor paxillin.