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. 2018 Feb 28;8:3773. doi: 10.1038/s41598-018-21885-x

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© The Author(s) 2018

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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The UPR and ISR markers are similarly induced in wt and 2b5^ho astrocytes upon short-term stress induction. UPR was induced by ER stressors tunicamycin (TM) or thapsigargin (TG). ISR was induced by treating cells with CCT020312 (CCT), BEPP, BTdCPU (BT) or halofuginone (HF) for 4 h. The kinases activated by ISR-inducing compounds are indicated (PERK, PKR, HRI or GCN2). The relative expression of mRNA markers of the UPR, Trib3, Xbp1s + u/u and Pdia4, was measured by qPCR after treatment. Values are fold change relative to vehicle-treated wt astrocytes. Graphs show average + SD (n = 3). P-values are shown in supplementary Table 1. Trib3, Xbp1s + u/u and Pdia4 are significantly increased by tunicamycin and thapsigargin while only Trib3 is significantly increased by CCT020312, BEPP, BTdCPU or halofuginone indicating ISR specificity. The increase is similar for wt and 2b5^ho astrocyte cultures.