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. 2020 Dec 7;52(12):1908–1925. doi: 10.1038/s12276-020-00535-1

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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 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. 2 — Pathological involvement of CASQ1 in skeletal muscle is summarized in circles (red). In the lower right (deep orange circles), diseases that are related to CASQ1 with no known mechanism are summarized. Corresponding proteins, mechanisms or phenomena are presented in parentheses. Pathological phenomena and tendencies due to the knockout of CASQ1 in mice are listed in the boxes. CASQ calsequestrin, RyR1 ryanodine receptor 1, SR sarcoplasmic reticulum, SOCE store-operated Ca²⁺ entry, MH malignant hyperthermia, EHS environmental/exertional heat stroke, TAM tubular aggregate myopathy, PAM protein aggregate myopathy, Ab antibody.