Platelet PI3Kβ and GSK3 regulate thrombus stability at a high shear rate

Author:

Laurent Pierre-Alexandre1,Séverin Sonia1,Hechler Béatrice2,Vanhaesebroeck Bart3,Payrastre Bernard14,Gratacap Marie-Pierre1

Affiliation:

1. INSERM, U1048 and Université Toulouse III, Institut de Maladies Métaboliques et Cardiovasculaires, Centre Hospitalier Universitaire-Rangueil, Toulouse, France;

2. Unité Mixte de Recherche-S949 INSERM-Université de Strasbourg, Établissement Français du Sang-Alsace, Strasbourg Cedex, France;

3. Cell Signalling, University College London Cancer Institute, Paul O'Gorman Building, University College London, London, United Kingdom; and

4. Centre Hospitalier Universitaire de Toulouse, Laboratoire d’Hématologie, Toulouse Cedex, France

Abstract

Key Points A key role for platelet PI3Kβ, but not α, and for GSK3 in thrombus stability at a high shear rate. Risk of platelet emboli formation on PI3Kβ inhibition in vivo.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

Reference42 articles.

1. Platelets and atherothrombosis: causes, targets and treatments for thrombosis.;Siddiqui;Curr Med Chem,2013

2. Antiplatelet therapies for the treatment of cardiovascular disease.;Michelson;Nat Rev Drug Discov,2010

3. The emerging mechanisms of isoform-specific PI3K signalling.;Vanhaesebroeck;Nat Rev Mol Cell Biol,2010

4. Coincidence detection in phosphoinositide signaling.;Carlton;Trends Cell Biol,2005

5. Pleckstrin homology (PH) domains and phosphoinositides.;Lemmon;Biochem Soc Symp,2007

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