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. 2020 Feb 18;11(2):125. doi: 10.1038/s41419-020-2324-4

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© The Author(s) 2020

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 6 — a Expressions of GRP78, p-PERK, PERK, ATF4, CHOP, Bcl-2, and Bax were determined by Western blotting after treatment with 100 ng/ml HMGB1 for 48 h. b, c Lentiviral vectors (SESN2 knockdown and SESN2 overexpression) were transduced DC2.4 cells, and scramble cells were transduced with blank vectors. After treated with 100 ng/ml HMGB1 for 48 h, expressions of GRP78, p-PERK, PERK, ATF4, and CHOP were determined by Western blot analysis. d The morphologic alteration of ER in each cell was evaluated by immunofluorescence staining and the extent of the ER morphologic change was compared with the scramble controls (×600, ×1200), scale bar = 25 μm, scale bar = 10 μm, n = 4 per group. ER was detected with ER-tracker red. β-actin served as the internal standard. Data were presented as the mean ± SD, n = 3 per group. Statistical significance: *P < 0.05 versus the control group.