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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. 4 — TAZ regulates mitochondrial fission. a, b Immunofluorescence staining of mitochondria. The average number of mitochondria was recorded. IL-2 treatment significantly activated mitochondrial fission, and this effect was further enhanced by TAZ deletion. c–f To quantify mitochondrial fission, the expression of mitochondrial fission-related proteins was analyzed. g Capsase-3 activity was measured in HepG2 cell transfected with TAZ siRNA in the presence of IL-2. To inhibit mitochondrial fission, Mdivi-1 was added to IL-2-treated cells. h–i PI staining was used to observe apoptotic cells. *P < 0.05 vs. control (Ctrl) group; ^#P < 0.05 vs. IL-2 group; ^@P < 0.05 vs. IL-2 + si-TAZ group