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. 2019 Dec 6;9:18557. doi: 10.1038/s41598-019-54931-3

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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RNF43-G659Vfs*41 inhibited Wnt signaling and reduced FZD levels as well as RNF43-WT could. (a) TOPFlash activity of STK-RZ-DKO cells transfected with vector (Vec), RNF43-WT, or –G659Vfs*41 in response to RPSO2 treatment. (b) WB of cells from (a) with anti-HA antibody. (c) WB of FZD5 in STK-RZ-DKO cells transfected with vector, RNF43-WT, or –G659Vfs*41 with anti-FLAG and anti-HA antibody. (d) WB of FZD5 of HEK293T cells transfected with vector, RNF43-WT, or G659Vfs*41 and treated with vehicle or RSPO2-Furin-Fc proteins (R2Fu) at 10 µg/ml. 1 = vehicle; 2 = RSPO2Fu-WT; 3 = RSPO2Fu-F109A. Actin and GAPDP were loading controls.