Figure 3.
Regression of PR-related phenotypes on PPR-associated variants. (A) log10 scale Q-Q plot comparing the P values obtained by regressing FC-derived PR to ADP, CRP-XL, PAR1-targeting peptide, and PAR4-targeting peptide on the imputed allele counts at 21 PPR-associated variants in 1373 PFC participants with the P values obtained under the null hypothesis of no association. The smallest P value obtained across agonists for each variant is highlighted using an agonist-specific color. (B) Heatmap showing the correlation structure among 48 in vitro phenotypes of thrombus formation and their relative loadings on the leading principal component of a principal components analysis. (C) Scatterplot of the scaled effect sizes of the 21 PPR-associated variants with respect to PPR in INTERVAL and the first principal component of the in vitro thrombus formation phenotypes in 87 PFC participants. The correlation (ρ) and the P value under the null hypothesis, ρ = 0, are embedded.

Regression of PR-related phenotypes on PPR-associated variants. (A) log10 scale Q-Q plot comparing the P values obtained by regressing FC-derived PR to ADP, CRP-XL, PAR1-targeting peptide, and PAR4-targeting peptide on the imputed allele counts at 21 PPR-associated variants in 1373 PFC participants with the P values obtained under the null hypothesis of no association. The smallest P value obtained across agonists for each variant is highlighted using an agonist-specific color. (B) Heatmap showing the correlation structure among 48 in vitro phenotypes of thrombus formation and their relative loadings on the leading principal component of a principal components analysis. (C) Scatterplot of the scaled effect sizes of the 21 PPR-associated variants with respect to PPR in INTERVAL and the first principal component of the in vitro thrombus formation phenotypes in 87 PFC participants. The correlation (ρ) and the P value under the null hypothesis, ρ = 0, are embedded.

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