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. 2024 May 13;10:227. doi: 10.1038/s41420-024-01984-7

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© The Author(s) 2024

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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Fig. 5 — Immunoblot analysis of pro-(P53), activated (P30) GSDMD, pro-(P53) and activated (P34) GSDME, pro-(P45) and activated (P20) CASP1; pro-(P35) and cleaved (P19 and P17) CASP3, pro-(P55) and cleaved (P18) CASP8, phosphorylated MLKL (pMLKL), phosphorylated RIPK1 (pRIPK1), and pro-(P75) and cleaved (P30) RIPK1, phosphorylated RIPK3 (pRIPK3), RIPK3 in DLD1, HCT116 (a, b, d–f), 293 T or HT29 (c) after co-treatment with IFN-γ and TNF-α or supplement with Emricasan, GSK'872, Z-IETD-FMK, VX-765 or Nec-1 for 24 h. ATP, GAPDH, and Lamin B1 were used as membrane, cytosolic, and nuclear internal control respectively. Data are representative of at least three independent experiments.