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. 2019 Apr 24;12:100. doi: 10.3389/fnmol.2019.00100

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Copyright © 2019 Di Pardo, Pepe, Castaldo, Marracino, Capocci, Amico, Madonna, Giova, Jeong, Park, Park and Maglione.

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) and the copyright owner(s) 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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Working model. Treatment with K6PC-5 stimulates the activity of SPHK1 with a subsequent increase in the levels of S1P. S1P may act either intracellularly, by stimulating autophagy and reducing mHtt aggregation, or extracellularly by stabilizing S1PR expression and activating pro-survival pathways.