Journal Article Ahead of print
PubMed: 42766692 DOI: 10.1182/blood.2026033425
JAK3 regulates PIP5K expression, promotes PIP2 generation and Ca2+ driven platelet activation in arterial thrombosis.
Blood
Authors: Patrick Münzer, Ferdinand Kollotzek, Mailin-Christin Manke, Betül Findik, Kristina Mott, Melina Fischer, Gundula D Lingens, Monika Zdanyte, Frederic Stein, Sascha Geue, Britta Walker, Meinrad Gawaz, Tobias Geisler, Dominik Rath, Robert Ahrends, Michael Lämmerhofer, Harald Schulze, Julia Skokowa, Oliver Borst
Affiliations
- University of Tübingen, Tübingen, Germany.
- Universitätsklinikum Tübingen, Tübingen, Germany.
- University Hospital Tuebingen, Tuebingen, Germany.
- University Hospital, University of Würzburg, Würzburg, Germany.
- Department of Cardiology and Angiology, Medizinische Klinik III, University Tuebingen, Germany, Tübingen, Germany.
- University Clinic Tuebingen, Tuebingen, Germany.
- University of Vienna, Institute of Analytical Chemistry, Vienna, Austria.
- University Hospital Wuerzburg, Wuerzburg, Germany.
- University of Tübingen, Tuebingen, Germany.
Abstract
Phospholipase C (PLC)-evoked rising intracellular Ca2+-levels are a prerequisite for platelet activation with subsequent thrombosis. The protein-tyrosine kinase Janus kinase 3 (JAK3) regulates phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2)-levels in platelets, thus significantly mediating activation-dependent platelet function and arterial thrombosis.
MeSH
Hematology, Protein-Tyrosine Kinases, Phosphatidylinositol 4,5-Diphosphate, Janus Kinases, Thrombosis, Blood Platelets, Platelet Activation