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. 2021 Apr 28;11:9188. doi: 10.1038/s41598-021-88610-z

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© The Author(s) 2021

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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dsRNA binding contributes to spontaneous activation of S6A-S97A PKR mutant. (a) Schematic representation of the main PKR domains. The coordinates on the top are those of the four lysines mutated to alanines in order to generate a DRBM-dead PKR (PKR-4KA). (b) PKR-KO cells were transfected with plasmids expressing PKR mutants and fixed 48 h post-transfection for eIF3 and PKR detection by immunofluorescence. Graphs (generated with Microsoft Excel 2011) show the mean and SEM of the percentages of stress granule-positive cells counted among PKR⁺ cells (n = 4). 1-way ANOVA (Graphpad Prism 7) compared each PKR condition to the S6A-S97A PKR mutant condition.