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. 2017 Dec 18;8:2168. doi: 10.1038/s41467-017-02351-0

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© The Author(s) 2017

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. 10 — The graphic illustration of the mechanism of SHP2 regulating NLRP3 inflammasome activation. Stimulated by Signal 2 activators (e.g., ATP, MSU, and Nigericin), SHP2 is recruited to mitochondria through its RRWFH motif. With the help of Tom20/Tom40 and Tim23 complex, SHP2 translocates into the mitochondrial matrix and dephosphorylates ANT1 at Tyr 191. This serves as a key mechanism controlling mitochondrial homeostasis, preventing leakage of mitochondrial DNA (mtDNA) and overproduction of reactive oxygen species (ROS), which results in negative regulation of NLRP3 inflammasome activation