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. 2019 May 22;218(6):1769–1770. doi: 10.1083/jcb.201904016

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© 2019 Van Den Bosch

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

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Figure 1. — Schematic illustration of the interaction between HDAC6 and Miro1. Nonpermissive substrates like MAG and CSPGs activate RhoA/ROCK, increase intracellular calcium, and induce the deacetylation of Miro1 at lysine 105 (K105). This decreases mitochondrial axonal transport and inhibits the outgrowth of the axonal growth cone. Selective inhibition of the deacetylase activity of HDAC6 using tubastatin A restores axonal transport, as well as all the other phenotypes. While the interaction with kinesin-1 is responsible for anterograde transport of the mitochondria, a similar mechanism might also be present for the retrograde transport machinery.