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. 2022 Jul 18;20:164. doi: 10.1186/s12915-022-01366-4

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© The Author(s) 2022

Open AccessThis 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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Ppargc1a expression in response to a Ca²⁺-mediated pharmacological exercise mimetic requires Tug1. A C2C12 myocytes were differentiated for 3 days then transfected with Tug1 or control LNA (25 nM) for 24 h. Transfected myotubes were then exposed to caffeine (0.1 mM), AICAR (0.5 mM), taurine (5 mM) or untreated control for 6 h, then B gene expression of Tug1 and Ppargc1a was analysed by RT-qPCR. Data are mean (SD) for n=6 (triplicate wells across two independent experiments), analysed by ordinary two-way ANOVA for main effects of LNA and treatment. Significant main interaction effect was analysed by Bonferroni post hoc test; **p<0.01, ***p<0.001, Tug1 KD vs. control (NC)