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. 2023 Nov 13;13:19750. doi: 10.1038/s41598-023-47111-x

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© The Author(s) 2023

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Predicted mechanism for RNF2 regulation of Wnt signaling through TCF7L1 ubiquitination. (a) Diagram of TCF7L1 deletion mutant used for the domain study. The image was generated using Adobe Illustrator software (version 27.3). (b) Western blot analysis was performed using control HeLa cells. A total of 6 μg of myc-TCF7L1 partial mutants and myc-RNF2 plasmids were introduced into cells, which were then lysed with RIPA buffer. (c) Proposed mechanism of the RNF2 regulation of Wnt signaling. RNF2 continuously degrades TCF7L1 through ubiquitination-mediated degradation to regulate TCF7L1 at low levels. TCF7L1 binding to a promoter region may avoid RNF2 ubiquitination. When Wnt is activated, TCF7L1 detaches from DNA and is exposed followed by the binding of ß-catenin and HIPK2 phosphorylation. Then, the TCF7L1 is degraded through RNF2-mediated ubiquitination. The image was generated using Adobe Illustrator software (version 27.3).