CLEC-2 induced signalling in blood platelets

   


1. Faculty of Physics, Lomonosov Moscow State University, Moscow, Russia; Center for Theoretical Problems of Physicochemical Pharmacology, Moscow, Russia
2. Faculty of Physics, Lomonosov Moscow State University, Moscow, Russia; Rogachev National Scientific and Practical Centre of Pediatric Hematology, Oncology and Immunology, Moscow, Russia
3. Center for Theoretical Problems of Physicochemical Pharmacology, Moscow, Russia; Rogachev National Scientific and Practical Centre of Pediatric Hematology, Oncology and Immunology, Moscow, Russia
Type: Review
DOI: 10.18097/PBMC20186405387      PubMed Id: 30378555
Year: 2018 vol: 64  issue:5  pages: 387-396
Abstract: Platelet activating receptor CLEC-2 has been identified on platelet surface a decade ago. The only confirmed endogenous CLEC-2 agonist is podoplanin. Podoplanin is a transmembrane protein expressed by lymphatic endothelial cells, reticular fibroblastic cells in lymph nodes, kidney podocytes and by cells of certain tumors. CLEC-2 and podoplanin are involved in the processes of embryonic development (blood-lymph vessel separation and angiogenesis), maintaining of vascular integrity of small vessels during inflammation and prevention of blood-lymphatic mixing in high endothelial venules. However, CLEC-2 and podoplanin are contributing to tumor methastasis progression, Salmonella sepsis, deep-vein thrombosis. CLEC-2 signalling cascade includes tyrosine-kinases (Syk, SFK, Btk) as well as adapter LAT and phospholipase Cg2, which induces calcium signalling. CLEC-2, podoplanin and proteins, participating in CLEC-2 signalling cascade, are perspective targets for antithrombotic therapy.
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Reference: Martyanov A.A., Kaneva V.N., Panteleev M.A., Sveshnikova A.N., CLEC-2 induced signalling in blood platelets, Biomeditsinskaya khimiya, 2018, vol: 64(5), 387-396.
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