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. 2017 Dec 8;2:17066. doi: 10.1038/sigtrans.2017.66

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Copyright © 2017 The Author(s)

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Schematic representation of the central role of MCPIP1 in LPS-induced inflammation and lung injury. As an RNase, MCPIP1 post-transcriptionally controls the production of cytokines and maintains inflammation at a basal level under physiological conditions. In response to inflammatory stimuli (for example, LPS), macrophage CARD9/BCL10/MALT1 signalosome is activated and MALT1 protease mediates MCPIP1 cleavage, which releases the ‘brake’ and initiates the inflammatory response. MI-2 specifically inhibits MALT1 protease activity and preserves the MCPIP1 protein levels, which can prevent/treat LPS-induced inflammation and lung injury.