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. 2022 May 15;8:44. doi: 10.1038/s41421-022-00403-4

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© The Author(s) 2022

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. 4 — a, b Magnified view of the interactions between TM3 and ICL2 of CCR2 (a) and CCR3 (b) with the α5-helix of Gα_i. c, d Detailed interactions of TM5, TM6, and ICL3 of CCR2 (c) and CCR3 (d) with the α5-helix of Gα_i. Green, CCL2-bound CCR2; pink, CCR3; yellow, Gα_i1. Hydrogen bonds are depicted as black dashed lines, and electrostatic bonds are depicted as red dashed lines. e, f Influence of single-site mutants of CCR2 (e) and CCR3 (f) on agonist-induced cAMP accumulation. n = at least three independent experiments performed with single replicates. The statistical difference between wild-type and mutated receptor was calculated by one-way ANOVA followed by Dunnett’s multiple comparisons test. Superscripts indicate statistically significant difference (*P < 0.01, ***P < 0.001, ****P < 0.0001; NS no significance). Bars are colored according to the extent of effect. All data are shown as means ± SEM. See Supplementary Tables S5 and S6 for detailed statistical evaluation.