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Proceedings of the National Academy of Sciences of the United States of America logoLink to Proceedings of the National Academy of Sciences of the United States of America
. 2020 Aug 17;117(34):20970–20971. doi: 10.1073/pnas.2015341117

Correction for Lin et al., Induction of USP25 by viral infection promotes innate antiviral responses by mediating the stabilization of TRAF3 and TRAF6

PMCID: PMC7456129  PMID: 32817540

IMMUNOLOGY AND INFLAMMATION Correction for “Induction of USP25 by viral infection promotes innate antiviral responses by mediating the stabilization of TRAF3 and TRAF6,” by Dandan Lin, Man Zhang, Meng-Xin Zhang, Yujie Ren, Jie Jin, Quanyi Zhao, Zishu Pan, Min Wu, Hong-Bing Shu, Chen Dong, and Bo Zhong, which was first published August 24, 2015; 10.1073/pnas.1509968112 (Proc. Natl. Acad. Sci. U.S.A. 112, 11324–11329).

The authors note the following: “The bright-field image of mock-infected Usp25−/− MEFs was accidentally overlaid by the bright-field image of NDV-infected Usp25+/+ MEFs (18 h) during the preparation and production process (Fig. 1E). This error does not affect the description of the results or the conclusion of this study. We apologize for the inconvenience caused.” The corrected Fig. 1 and its legend appear below.

Fig. 1.

Fig. 1.

USP25 positively regulates RNA virus-induced signaling in primary mouse embryonic fibroblasts (MEFs). (A) The expression of Ifnb, Ifna4, Tnf, and/or Il6 was inhibited in Usp25−/− MEFs than in wild-type counterparts after SeV or VSV infection or transfection of the dsRNA analog poly(I:C). Wild-type or Usp25−/− MEFs were infected with SeV or VSV or transfected with poly(I:C) (1 μg) for the indicated time points before qPCR analysis was performed. (B) Usp25−/− MEFs produced decreased amount of IFN-α, IL-6, and TNF-α proteins after SeV or VSV infection than did the wild-type cells. Wild-type or Usp25−/− MEFs were infected with SeV or VSV for the indicated time points and the supernatants were collected for ELISA analysis. (C) SeV- or VSV-induced phosphorylation of IRF3 and IκBα was substantially impaired in Usp25−/− MEFs. Wild-type or Usp25−/− MEFs were infected with SeV or VSV for the indicated time points. Cells were lysed and the cell lysates were subject to immunoblot analysis with the indicated antibodies. (D and E) The replication of GFP-tagged Newcastle disease virus (NDV) was potentiated in Usp25−/− MEFs compared with the wild-type MEFs. Wild-type or Usp25−/− MEFs were infected with GFP-NDV (MOI = 0.01, D; MOI = 0.1, E) for 18 or 24 h. Cells were harvested for flow cytometry or microscopy imaging and immunoblot analysis. Data are representative of three independent experiments (mean and SD of three replicates in A and B).


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