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. 2016 Jan 25;6:5. doi: 10.1186/s13578-016-0070-1

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© Xue et al. 2016

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. 5 — Effect of CLIC4 on the Ca²⁺ store release. Representative traces (a and c) and summarized data (b and d) showing 100 μmol/L ATP− (a and b) and 2 μmol/L thapsigargin (TG, c and d) -induced HN4 cell intracellular Ca²⁺ ([Ca²⁺]_i) rise in Ca²⁺-free saline solution. [Ca²⁺]_i was detected by the cell-permeable Ca²⁺-sensitive fluorescent indicator Fluo-8 AM. The change in [Ca²⁺]_i was indicated by the ratio of the fluorescence density before and after the application of agonists. The HN4 cells were transfected with CLIC4 (CLIC4 siRNA) or scrambled (Con) siRNA. Values are shown as the mean ± SE. n = 5. *P < 0.05. vs. the control (Con) group