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. 2019 Feb 28;9:3135. doi: 10.1038/s41598-019-40008-8

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© The Author(s) 2019

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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Improvement in the TGF-α shedding response to OAD in HEK293 cells expressing P2Y1, P2Y4, P2Y6, P2Y10, P2Y11, CB1, and CB2. (A) Summary of the results of the TGF-α shedding response in cells transfected with P2Y receptors during the screening series. Mock transfected cells (pCAGGS empty vector) (white bar) (B–H) or HEK 293 cells expressing GPCRs (left) (P2Y1 (B,H), human P2Y6 (C, dark bar), mouse P2Y6 (B, red bar), P2Y10 (D), P2Y11 (E,H), CB1 (F), CB2 (G), and human and mouse P2Y4 (H)) were treated with OAD (right) or each receptor agonist (left) (ADP (B), UDP (C), LysoPS (D), ATP (E), CP-55940 (F,G)). The TGF-α shedding response was then calculated. Data represent the mean (n = 2) (A,B, D–F), mean ± S.E.M (n = 4) (C), or mean ± S.E.M (n = 3) (H).