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. 2017 Jul 18;7:5650. doi: 10.1038/s41598-017-05995-6

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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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Loss of CG17259 induced eIF2α phosphorylation. (a) The quantitative RT-PCR for Xbp1 _FL is shown. The DNA gel with migrations of Xbp1 _FL and Xbp1 _sp are indicated. Xbp1 _sp is not detected. Trial n = 8. (b) The Western blot shows the level of phosphorylated form of eIF2α (eIF2α-p) in the CG17259 mutant flies. The eIF2α-p antibody recognizes the S51 phosphorylation site of eIF2a. Actin is shown as the protein loading control. Trial n = 3. The full length gels of all Western blots were shown at the end of the supplementary information. (c) The Western blot shows the level of GluR1^Lc in the genotype of flies indicated. Actin is shown as the protein loading control. Trial n = 3. (d) The Western blot shows the level of eIF2α-p in the Gadd34 mutant flies. Actin is shown as the protein loading control. Trial n = 3. (e) Survival rate of AG flies was shown with the genotype of flies indicated. Trial n = 4.