Journal of Cell Biology volume 218, issue 6, P1871-1890 2019 DOI: 10.1083/jcb.201702187 View full text
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Ashley L. Kalinski, Amar N. Kar, John Craver, Andrew P. Tosolini, James N. Sleigh, Seung Joon Lee, Alicia Hawthorne, Paul Brito-Vargas, Sharmina Miller-Randolph, Ryan Passino, Liang Shi, Victor S.C. Wong, Cristina Picci, Deanna S. Smith et al.

Abstract: Extracellular stimuli in the injured CNS, such as chondroitin sulfate proteoglycans, inhibit axon growth through activation of the small GTPase RhoA. This RhoA activation increases intracellular Ca2+ that converges on an HDAC6-dependent pathway to deacetylate Miro1. Deacetylation of Miro1 decreases mitochondrial transport and attenuates axon growth.