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. 2013 Mar 18;121(20):4205–4220. doi: 10.1182/blood-2012-08-449272

Figure 1.

Figure 1

Figure 1

Figure 1

Aberrant function of Shp1- and Shp2-deficient platelets. (A) Platelet counts and volumes from Shp1 KO (n = 37), Shp2 KO (n = 43), Shp1/2 DKO (n = 11), and litter-matched wild-type mice (Shp1 WT, n = 36; Shp2 WT, n = 39; Shp1/2 WT, n = 7). Mean ± SEM; **P < .01, ***P < .001. (B-C) Aggregation and ATP secretion of washed platelets were measured by lumi-aggregometery in response to agonists indicated. (i) Representative traces, n = 4-8 mice/genotype per condition. (ii) Data presented are means (±SEM) of 3 independent experiments (***P < .001). (D) P-selectin expression and fibrinogen binding of (i) Shp1/2 DKO, (ii) Shp1 KO, and (iii) Shp2 KO platelets in whole blood in response to 3 μg/mL CRP, 3 μg/mL convulxin, and 500 μM PAR-4 peptide (PAR4). Geometric mean fluorescence intensity (MFI) ± SD, n = 4-8 mice/genotype per condition, except convulxin-stimulated Shp1/2 DKO conditions, which are n = 2; **P < .01.