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. Author manuscript; available in PMC: 2010 Dec 1.
Published in final edited form as: Expert Rev Hematol. 2010 Feb;3(1):81–91. doi: 10.1586/ehm.09.75

Table 1.

Effects of genetic deletion/modification of Akt isoforms or its regulatory proteins in platelets.

Mouse model Defect in sensitivity to agonists Effect on Akt phosphorylation Effect on platelet function Ref.
Akt1 −/−
Collagen, thrombin

Reduces calcium release, aggregation and hemostasis (increases tail-bleeding time)
[6]
Akt2 −/−
PAR4 agonist, ADP

Reduces aggregation, secretion and thrombosis in carotid artery injury model
[5]
PI3Kβ KD
ADP, thromboxane A2 (U46619), glycoprotein VI agonist
Decrease
Reduces platelet aggregation, adhesion and spreading on fibrinogen
[66]
PI3K γ −/− ADP Decrease Reduces maximal ADP aggregation [63,64]
ADP No change Reduces maximal ADP aggregation [65]



Reduces response to arterial injury model of thrombosis, thromboembolism
[63,64]
PI3Kγ KD ADP, thromboxane A2 (U46619) Decrease Reduces aggregation [66]