We have generated transgenic mice overexpressing the human P2X1 ion channel in the megakaryocytic cell lineage. Platelets from transgenic mice exhibited a gain of P2X1 ionotropic activity as determined by more prominent P2X1– mediated Ca2+ influx and platelet shape change.

P2X1 overexpression enhanced platelet secretion and aggregation evoked by collagen, convulxin, a GPVI-selective agonist, or the thromboxane A2 mimetic U46619.

In contrast, these platelet responses to ADP and thrombin were normal.

Hence, the platelet P2X1 ion channel plays a role in hemostasis and thrombosis through its participation in collagen-, thromboxane A2 and shear stress-triggered platelet responses. Activation of the ERK2 pathway is instrumental in these processes.

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