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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 1. — SIAH proteins positively regulate Wnt/β-catenin signaling. (A) Depletion of SIAH1 by independent siRNAs inhibits Wnt3a-induced STF reporter in HEK293 cells. pGL2 nontargeting siRNA served as a negative control. Error bars denote the SD between four replicates. (B) Depletion of SIAH1 by siRNA attenuates Wnt3a-induced cytosolic β-catenin accumulation. The intensity of the β-catenin band was quantified by ImageJ. (C) Knockout of SIAH1 by CRISPR attenuates Wnt3a-induced STF-GFP reporter in HEK293 cells. The FACS plot is a representative from three independent experiments. (D) Knockout of SIAH1 by CRISPR attenuates Wnt3a-induced cytosolic β-catenin accumulation. (E) Overexpression of wild-type Siah1a and SIAH2, but not their RING domain mutants, enhances Wnt3a-induced STF reporter in HEK293 cells. Error bars denote the SD between four replicates. (F,G) Overexpression of wild-type Siah1a or SIAH2 enhances Wnt3a-induced accumulation of cytosolic β-catenin.