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. 2022 Nov 3;5:1176. doi: 10.1038/s42003-022-04120-2

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© The Author(s) 2022

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. 5 — a Increasing amounts of different NLRP3 variants targeting the AAA+ ATPase fold were transiently over-expressed in HeLa cells stably over-expressing ASC-mTurquoise. ASC specks and nuclei were quantified using microscopy, and the ratio ASC speck/nuclei was plotted as a measure of inflammasome activation. Bars represent mean and SD of 5 independent experiments. b Dose response curves for the active NLRP3 mutants described in a. The half maximal effective concentration (EC50) was calculated for each of the NLRP3 variants. Data points of 5 independent experiments are shown. c, d NLRP3-deficient immortalized macrophages were reconstituted with wildtype NLRP3-mCitrine or indicated variants. c TNF-α and d IL-1β secretion of LPS primed immortalized macrophages stimulated with nigericin in the presence or absence of CRID3. Means ±SEM of pooled data from 3 independent experiments are presented.