Defects in secretion, aggregation, and thrombus formation in platelets from mice lacking Akt2
J. Clin. Invest. Donna Woulfe, et al. 113:441 doi:10.1172/JCI20267 [
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Figure 1Phosphorylation of Akt and GSK-3β in WT,
Akt1–/–, and
Akt2–/– mice. Washed platelets (2 × 107 platelets in 100 μl) were stimulated for 10 minutes with buffer alone (untxd), thrombin (thr; 1 U/ml), or thrombin in the presence of the PI3K inhibitor, LY294002 (thr + LY; 50 μM) and then immunoblotted with Ab’s directed against (
a) Akt phosphorylated on serine 473 (Akt-PSer473), (
b) total Akt, (
c) GSK-3β phosphorylated on serine 9 (GSK-3β–PSer9), and (
d) total GSK-3β. The results shown are representative of those obtained a minimum of three times.
