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. 2021 Oct 18;40(47):6469–6478. doi: 10.1038/s41388-021-02059-y

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© The Author(s) 2021

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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Fig. 1 — A In the absence of canonical Wnt ligands the central destruction complex induces β-catenin degradation, restraining the transcription of Wnt target genes. B Canonical Wnt ligands induce dissociation of β-catenin from the degradation complex, leading to β-catenin accumulation, nuclear translocation and transcription of Wnt target genes. Ubiquitin ligases ZNRF3/RNF43 negatively regulate the Wnt pathway by internalizing and degrading membrane receptors LRP5/6 and FZD, thereby reducing Wnt receptor availability at the membrane. C RSPOs potentiate the canonical Wnt pathway by clearing negative regulators ZNRF3/RNF43 from the membrane, thereby increasing membranous Wnt receptor availability and potentiation of Wnt ligand-mediated pathway activation.