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. 2023 Mar 8;132(7):828–848. doi: 10.1161/CIRCRESAHA.122.321448

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© 2023 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited.

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Figure 1. — Analysis of the β-adrenergic phosphoproteome selectively elicited by inhibition of PDE3 (phosphodiesterase 3) or PDE2A. A, Frequency distributions of log2 intensity ratios to illustrate thresholding of PDE3-dependent and PDE2A-dependent (B) phosphoproteomics data for pathway analysis. The top 16% quantified phosphopeptides (highlighted in green and purple for PDE3A and PDE2A, respectively) were carried forward for further analysis. C, Venn diagram comparing the 16% upregulated phosphorylation sites in samples treated with the PDE3 inhibitor (green) or the PDE2A inhibitor (purple). The CI (68%) derives from the selected peptides lying outside 1 SD of the mean distribution of peptides, as shown in A and B, respectively. BAY indicates BAY 60-7550; Cilo, cilostamide; and Iso, isoproterenol.