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. 2023 Jul 27;30(10):1403–1413. doi: 10.1038/s41417-023-00647-6

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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 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. 4 — A HCT116 and DLD-1 cells were treated with WNT3A for 2 h and IB analysis for detection of RIP1, β-catenin, cIAP1, and cIAP2 was performed. β-Actin was used as the loading control. B IB analysis of RIP1 and β-catenin in HCT116 and DLD-1 cells transfected with siRNAs against cIAP1 (sicIAP1) or cIAP2 (sicIAP2) or control siRNA (siCon), followed by treatment with WNT3A. C HCT116 and DLD-1 cells were immunoprecipitated with β-catenin antibody, and then IB analysis was performed with anti-cIAP1 and cIAP2. D Ubiquitylation assay performed with DLD-1 cells transfected with sicIAP1, sicIAP2 or siCon, followed by sequential treatment with WNT3A with or without 10 μM MG132.