Title : Resistance to thromboembolism in PI3Kgamma-deficient mice.

Pub. Date : 2001 Sep

PMID : 11511514






5 Functional Relationships(s)
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1 When platelets from mice lacking the G protein-activated PI3Kgamma isoform were stimulated with ADP, aggregation was impaired. Adenosine Diphosphate phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus
2 ADP stimulation of PI3Kgamma-deficient platelets resulted in decreased PKB/Akt phosphorylation and alpha(IIb)beta(3) fibrinogen receptor activation. Adenosine Diphosphate phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus
3 These effects did not influence bleeding time but protected PI3Kgamma-null mice from death caused by ADP-induced platelet-dependent thromboembolic vascular occlusion. Adenosine Diphosphate phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus
4 This result demonstrates an unsuspected, well-defined role for PI3Kgamma downstream of ADP and suggests that pharmacological targeting of PI3Kgamma has a potential use as antithrombotic therapy. Adenosine Diphosphate phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus
5 This result demonstrates an unsuspected, well-defined role for PI3Kgamma downstream of ADP and suggests that pharmacological targeting of PI3Kgamma has a potential use as antithrombotic therapy. Adenosine Diphosphate phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma Mus musculus