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. 2022 Oct 5;5:1060. doi: 10.1038/s42003-022-04034-z

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© The Author(s) 2022

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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Fig. 3 — a–h Volcano plots for different pathways indicating changes in gene expression due to loss of Grpel1 in skeletal muscle. i Graphical representation of crosstalk between dysfunctional mitochondrial, due to loss of Grpel1, with other cellular organelles. Red color (arrows) indicates upregulation whereas the blue color (arrows) indicates downregulation (Created with BioRender.com). j Immunoblot of total protein lysates from QF muscle of Grpel1^skm−/−, Grpel1^flox/flox and WT mice. k–n Quantification of p-EIF2α level, p-EIF2α/total EIF2α ratio, p-S6 level and p-S6/total S6 ratio in skeletal muscle of Grpel1^skm−/−, Grpel1^flox/flox and WT mice. Vinculin was used as the loading control (n = 3 per genotype).