期刊
HAMOSTASEOLOGIE
卷 38, 期 4, 页码 210-222出版社
GEORG THIEME VERLAG KG
DOI: 10.1055/s-0038-1675149
关键词
platelet signaling; integrin alpha IIb beta 3; G protein-coupled receptors; calcium mobilization
类别
资金
- German Research Council (DFG
- Collaborative Research Center, SFB 612) [Scha 358/1-1, Scha 358/1-2, Scha 358/1-3, 358/2-2, 358/3-1]
- Biological Medical Research Center, Heinrich Heine University, Dusseldorf, Germany
- NRW Research School BioStruct 'Biological Structures in Molecular Medicine and Biotechnology'
Platelet signal transduction is the focus of this review. While 'classic' platelet signaling through G protein-coupled receptors in response to fluid-phase agonists has been extensively studied, signaling mechanisms linking platelet adhesion receptors such as GPIb-IX-V, GPVI and alpha 2 beta 1 to the activation of alpha IIb beta 3 are less well established. Moreover, 'non-haemostatic' pathways can also activate platelets in various settings, including platelet-immune or platelet-tumour cell interactions, platelet responses to neutrophil extracellular traps, or stimulation by microbial pathogens. Genetically determined integrin variants canmodulate platelet function and increase thrombogenicity. A typical example is the Pro33 (HPA-1b) variant of alpha IIb beta 3. Recent advances in the genotype-phenotype relation of this prothrombotic variant and its impact on outside-in signaling will be reviewed.
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