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. 2019 Oct 2;9:979. doi: 10.3389/fonc.2019.00979

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Copyright © 2019 Yu, Ding, Liang, Zhang and Chen.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Multiple types of stimulatory signals can activate NLRP3 to form a macromolecular signaling complex with its adaptor protein ASC, which causes the cleavage of pro-caspase-1 to the active form of caspase-1, which in turn transforms pro-IL-1β and pro-interleukin (IL)-18 into their biologically active, mature secreted forms. Furthermore, TIF1γ can ubiquitinate and assist DHX33 to interact with, and activate NLRP3 to form a macromolecular signaling complex to produce mature IL-1β and IL-18.