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. 2019 Jul 30;13:350. doi: 10.3389/fncel.2019.00350

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Copyright © 2019 Zamponi and Pigino.

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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Common molecular mechanism of fast axonal transport inhibition shared by oPrP^C and oAβ-42. Cellular and pharmacological data determined that both oPrP^C and oAβ-42 induced fast axonal transport inhibition. The inhibitory mechanism was mediated by the activation of endogenous CK2 and GSK3β that in turn phosphorylated KLCs. Phosphorylation of KLCs (letter P on KLCs) promoted the detachment of conventional kinesin from its transported vesicular cargoes. We and others have shown that CK2 can also phosphorylate kinesin-1 heavy chains (KHCs) (letter P on KHCs). Based on our previous results working with KHCs phosphorylation, we predict an additional mechanism of fast axonal transport inhibition induced by CK2 phosphorylation on KHCs which in turn will promote a reduction of kinesin-1 association to microtubules (MTs).