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. 2019 Dec 17;10:5754. doi: 10.1038/s41467-019-13623-2

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© The Author(s) 2019

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. 5 — a Representative images of MEF2 localization in cardiomyocytes treated with FCS or PE for 48 h. Scale bar, 20 μm. b Representative images of HDAC9 localization in cardiomyocytes cultured with or without FCS. Scale bar, 100 μm. c Representative images of PI4P accumulation in cardiomyocytes. Scale bar, 20 μm. d Representative images of GM130 distribution in cardiomyocytes. Scale bar, 50 μm. e Effects of a PKD activator (ilimaquinone (IQ)) and a PKD inhibitor (CID755673) on GM130 distribution in control and FKTN-deficient (KO) HEK cells. Arrowheads show abnormally distributed GM130 signals. Scale bar, 100 μm. f Representative images of GM130 distribution in control (mock), FKTN-deficient (fukutin-KO), and rescued (fukutin-KO transfected with pcDNA-FKTN-FLAG) HAP cells. Arrowheads show abnormally distributed GM130 signals. Scale bar, 100 μm.