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. 2020 May 25;11:513. doi: 10.3389/fphys.2020.00513

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Copyright © 2020 Hoshi.

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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Summary of events induced by valproic acid treatment on Kv7.2 channel complex. (A) Valproic acid treatment inhibits S-palmitoylation of AKAP79/150. Palmitoylation-deficient AKAP79/150 cannot mediate PKC phosphorylation of Kv7.2 subunit, which preserves M-current during seizures. (B) Summary of S-palmitoylation cycle and a potential action of valproic acid in this process. Valproic acid treatment may deplete free cytosolic CoA and interfere with generation of palmitoyl-CoA. A similar mechanism may be applicable to MCT therapy. See text for detail.