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. 2017 May 1;31(9):904–915. doi: 10.1101/gad.300053.117

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© 2017 Ji et al.; Published by Cold Spring Harbor Laboratory Press

This article is distributed exclusively by Cold Spring Harbor Laboratory Press for the first six months after the full-issue publication date (see http://genesdev.cshlp.org/site/misc/terms.xhtml). After six months, it is available under a Creative Commons License (Attribution-NonCommercial 4.0 International), as described at http://creativecommons.org/licenses/by-nc/4.0/.

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Figure 6. — Inhibition of SIAH1 blocks Wnt-induced Axin ubiquitination and degradation. (A) Wnt3a induces ubiquitination of endogenous AXIN1 in a time-dependent manner. HEK293 cells were pretreated with MG132 to prevent Wnt-induced AXIN1 degradation. (B) Wnt3a decreases the interaction between AXIN1 and GSK3β. Cells were pretreated with MG132 to prevent Wnt-induced Axin degradation and then treated with Wnt3a for 4 h. (C,D) Depletion or knockout of SIAH1 inhibits Wnt3a-induced ubiquitination of AXIN1. (E,F) Depletion or knockout of SIAH1 attenuates Wnt3a-induced AXIN1 degradation and cytosolic β-catenin accumulation. (G) A schematic model of Wnt-induced degradation of Axin through SIAH.