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. 2018 Jan 9;8:166. doi: 10.1038/s41598-017-18452-1

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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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Proposed model for the P5-mediated inhibition of HMGB1 release. Prolonged stimulation with crude LPS or SAA led to the up-regulation of Cx43, which may contribute to extracellular ATP efflux, P2X₇R-mediated PKR phosphorylation, and resultant PKR-mediated pyroptosis and HMGB1 release. As a novel Cx43 inhibitor, the P5 peptide may block the LPS/SAA-induced ATP efflux, thereby impairing the PKR-mediated HMGB1 release.