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. 2018 Feb 6;9(17):13593–13611. doi: 10.18632/oncotarget.24423

Figure 4. Affinities of AR agonists and antagonists in different cells expressing A2A and A2BARs.

Figure 4

(A) Competition binding experiments of agonists versus 1 nM [³H]MSX-2 at A2A-expressing membranes, and versus 0.3 nM [³H]PSB-603 at A2B- and at A2A-A2BAR-expressing membranes of CHO cells. The two-tailed t-test showed significant differences. ***p < 0.001, **p < 0.01, n = 2–3, see also Supplementary Table 3. (B) Competition binding experiments of AR antagonists versus 1 nM [³H]MSX-2 at A2A-expressing, and versus 0.3 nM [³H]PSB-603 at A2B - and at A2A-A2BAR co-expressing CHO cell membranes. The two-tailed t-test showed significant differences. ***p < 0.001, *p < 0.1, n = 3, see also Supplementary Table 3. (C) Competition binding experiments of AR agonists and antagonists versus 0.3 nM [³H]PSB-603 at Jurkat-T and HeLa cell membranes, n = 3–6, see also Supplementary Table 3. (D) Competition binding experiments agonists and antagonists versus 5 nM [³H]CGS-21680, and versus 1 nM [³H]MSX2, respectively, at HeLa cell membranes recombinantly overexpressing A2AARs. The two-tailed t-test showed significant differences. ns: not significant, ***p < 0.001, n = 3–4, see also Supplementary Table 3.