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. 2021 Nov 16;12(12):1088. doi: 10.1038/s41419-021-04378-0

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© The Author(s) 2021

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. 2 — A mRNA expression of P2X7A and P2X7B in Sk-Mel-28 cells evaluated by real time-PCR (N = 4). B mRNA expression of P2X7A and P2X7B in Ma-Mel-19 cells evaluated by real-time PCR (N = 4). P2X7 receptor activity as a channel was evaluated in C Sk-Mel-28 cells and D Ma-Mel-19 cells by measuring variations in [Ca²⁺]_I following stimulation with P2X7R agonist BzATP (300 μM). The P2X7 receptor antagonists A740003 (20 μM) and AZ10606120 (2 μM) completely obliterated the effect of BzATP. P2X7 activity as a large solute (up to 900 Da) pore was evaluated in E Sk-Mel-28 cells and F Ma-Mel-19 cells by measuring ethidium uptake following stimulation with BzATP (300 μM). The P2X7 receptor antagonists A740003 (20 μM) and AZ10606120 (2 μM) blocked the effect of BzATP.