CK2β regulates thrombopoiesis and Ca2+-triggered platelet activation in arterial thrombosis

Author:

Münzer Patrick1,Walker-Allgaier Britta1,Geue Sascha1,Langhauser Friederike2,Geuss Eva2,Stegner David3,Aurbach Katja34,Semeniak Daniela34,Chatterjee Madhumita1,Gonzalez Menendez Irene5,Märklin Melanie6,Quintanilla-Martinez Leticia5,Salih Helmut R.67,Litchfield David W.8,Buchou Thierry9,Kleinschnitz Christoph210,Lang Florian111,Nieswandt Bernhard3,Pleines Irina34,Schulze Harald34,Gawaz Meinrad1,Borst Oliver1

Affiliation:

1. Department of Cardiology and Cardiovascular Medicine, University of Tübingen, Tübingen, Germany;

2. Department of Neurology, University of Würzburg, Würzburg, Germany;

3. Rudolf Virchow Center, Research Center for Experimental Biomedicine, Würzburg, Germany;

4. Institute for Experimental Biomedicine, University of Würzburg, Würzburg, Germany;

5. Department of Pathology, and

6. Department of Hematology and Oncology, University of Tübingen, Tübingen, Germany;

7. Clinical Cooperation Unit Translational Immunology, German Cancer Consortium, German Cancer Research Center Partner Site Tübingen, Tübingen, Germany;

8. Department of Biochemistry, University of Western Ontario, London, ON, Canada;

9. INSERM, Institute for Advanced Biosciences, University Joseph Fourier Grenoble, La Tronche, France;

10. Department of Neurology, University of Essen, Essen, Germany; and

11. Department of Physiology, University of Tübingen, Tübingen, Germany

Abstract

Key Points CK2β is critically required for thrombopoiesis by regulating tubulin polymerization, MK fragmentation, and proplatelet formation. CK2β facilitates inositol triphosphate–mediated increase of cytosolic Ca2+ and is essential for platelet activation in arterial thrombosis in vivo.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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