Figure 3
Figure 3. Mass spectrometry analysis of aspirin-treated releasate. The complete number of proteins identified and the number of spectral counts for each condition is available in Table S1. Spectral counts (top) and extracted ion currents (XICs; bottom) for representative ions from thrombospondin (FASAEAEEDGDLQCLCVK, GKEESLDSDLYAELR, EAEEDGDLQCLCVK) and platelet factor 4 (FTGSQPFGQGVEHATANK, RPPLCYHNGVQYR, TIVTTLQDSIR) (errors bars are SD for mean of peptide XICs) indicated that the abundance of these proteins was decreased in the aspirin-treated fractions (A). Hierarchical clustering of agonist-induced platelet releasate protein profiles in the presence or absence of aspirin was perfomed. Spectral counts for each fraction were tabulated and null values were replaced with the value 0.01. The data were normalized across samples, log-transformed, and clustered using the Spearman rank correlation coefficient (average linkage) using Cluster 3.0 (B).

Mass spectrometry analysis of aspirin-treated releasate. The complete number of proteins identified and the number of spectral counts for each condition is available in Table S1. Spectral counts (top) and extracted ion currents (XICs; bottom) for representative ions from thrombospondin (FASAEAEEDGDLQCLCVK, GKEESLDSDLYAELR, EAEEDGDLQCLCVK) and platelet factor 4 (FTGSQPFGQGVEHATANK, RPPLCYHNGVQYR, TIVTTLQDSIR) (errors bars are SD for mean of peptide XICs) indicated that the abundance of these proteins was decreased in the aspirin-treated fractions (A). Hierarchical clustering of agonist-induced platelet releasate protein profiles in the presence or absence of aspirin was perfomed. Spectral counts for each fraction were tabulated and null values were replaced with the value 0.01. The data were normalized across samples, log-transformed, and clustered using the Spearman rank correlation coefficient (average linkage) using Cluster 3.0 (B).

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