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. 2016 Oct 19;10:459. doi: 10.3389/fnins.2016.00459

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Copyright © 2016 Vallée and Lecarpentier.

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) or licensor 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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A schematic model of the Wnt/beta-catenin pathway. In the Wnt “on state” (right part), Wnt binds both Fzd and LRP5/6 receptors to initiate LRP phosphorylation as well as Dsh/Fzd internalization. Dsh membrane translocation leads to dissociation of the axin/APC/GSK-3β complex. Beta-catenin phosphorylation is inhibited and it accumulates in the cytosol. The cytosolic beta-catenin translocates to the nucleus and binds to TCF/LEF factors. This results in the Wnt-responsive gene transcription. In Wnt “off state” (left part), Dsh dissociates from Fzd and Axin. APC and axin complex with GSK-3β. Beta-catenin is phosphorylated, dissociates from GSK-3β, migrates to the cytosol and is destroyed in the proteasome. Abbreviations: APC, adenomatous polyposis coli; Dsh, Disheveled; Fzd, Frizzled; GSK-3β, glycogen synthase kinase-3beta; LRP5/6, low density lipoprotein receptor-related protein 5/6; TCF/LEF, T-cell factor /lymphoid enhancer factor.