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. 2016 May 9;2:16010. doi: 10.1038/cddiscovery.2016.10

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Copyright © 2016 Cell Death Differentiation Association

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/

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Characterization of the OR51B5-mediated intracellular signaling components. (a) Under Ca²⁺-free conditions, an increase in cytosolic Ca²⁺ levels during isononyl alcohol stimulation was almost completely abolished. (b) During the co-treatment with isononyl alcohol and the AC inhibitor SQ-22536, no Ca²⁺ signals could be detected. (c) The PKA inhibitor H-89 blocked the isononyl alcohol-induced increase in intracellular Ca²⁺. (d) The PLC inhibitor U73122 could not significantly block the isononyl alcohol-mediated Ca²⁺ increase. (e) L-type calcium channel inhibitor Verapamil abolished the isononyl alcohol-induced Ca²⁺ increase in K562 cells. (f) The inhibitor experiments were analyzed relative to the first and second applications of isononyl alcohol.