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. 2018 Aug 14;18:117. doi: 10.1186/s12935-018-0615-y

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© The Author(s) 2018

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 6 — TAZ modulates mitochondrial fission via the JNK/F-actin pathway. a–c Western blotting was used to analyze JNK activity and F-actin expression. IL-2 treatment promoted JNK phosphorylation and F-actin upregulation; this effect was further enhanced by TAZ deletion. To inhibit the activity of JNK, SP600125 (SP) was added to TAZ-depleted cells. To activate the JNK pathway, anisomycin (Ani) was added to control cells. d, e Immunofluorescence staining of phosphorylated JNK following TAZ deletion and IL-2 treatment. f, g Immunofluorescence staining for F-actin following JNK activation or inhibition. h, i Immunofluorescence staining of mitochondria. The average number of mitochondria was recorded. *P < 0.05 vs. control (Ctrl) group; ^#P < 0.05 vs. IL-2 group; ^@P < 0.05 vs. IL-2 + si-TAZ group