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. 2018 Mar 8;19(3):770. doi: 10.3390/ijms19030770

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© 2018 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Model of the lithium-response pathway in bipolar disease. CRMP2 (collapsin response mediator protein-2) is a major target of GSK3β (glycogen synthase kinase). This enzyme catalyzes phosphorylation of the threonine (T) residue 154 in CRMP2. This step associates with CRMP2 inactivation in human neuronal progenitor cells and mature neurons. Conversely, inhibition of GSK3β by lithium prevents CRMP2 inactivation and supports its role in axon guidance and cytoskeletal dynamics. Interestingly, the ratio of CRMP2-pT154:CRMP2 is higher in neurons from lithium responsive (LR) patients and is normalized under lithium (Li) treatment.