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. 2016 Jun 2;7(6):e2239. doi: 10.1038/cddis.2016.146

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Copyright © 2016 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. 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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A hypothetical model of TMEM2 exerting its antiviral functions. TMEM2 activates the JAK–STAT signaling pathway and regulates the levels of p-Tyk2, p-JAK1, p-STAT1, p-STAT2, MxA and OAS1 in HepG2 and HepG2.2.15 cells. IFN can also activate the JAK–STAT signaling pathway and upregulate TMEM2 expression, leading to enhanced inhibitory effects of IFN on HBV production. Furthermore, TMEM2 increases the translocation of IRF9 into nuclei, thus enhancing the expression of a luciferase reporter gene under the control of ISRE motifs