CLEC-2 induced signalling in blood platelets

   
Martyanov A.A.1 , Kaneva V.N.2, Panteleev M.A.3, Sveshnikova A.N.1

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
Section: Review
DOI: 10.18097/PBMC20186405387      PubMed Id: 30378555
Year: 2018  Volume: 64  Issue: 5  Pages: 387-396
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.
Download PDF:  
Keywords: platelet, CLEC-2 receptor, tyrosine kinases, lymphangiogenesis, methastasis, podoplanin
Citation:

Martyanov, A. A., Kaneva, V. N., Panteleev, M. A., Sveshnikova, A. N. (2018). CLEC-2 induced signalling in blood platelets. Biomeditsinskaya Khimiya, 64(5), 387-396.
This paper is also available as the English translation: 10.1134/S1990750819010074
References  
 2024 (vol 70)
 2023 (vol 69)
 2022 (vol 68)
 2021 (vol 67)
 2020 (vol 66)
 2019 (vol 65)
 2018 (vol 64)
 2017 (vol 63)
 2016 (vol 62)
 2015 (vol 61)
 2014 (vol 60)
 2013 (vol 59)
 2012 (vol 58)
 2011 (vol 57)
 2010 (vol 56)
 2009 (vol 55)
 2008 (vol 54)
 2007 (vol 53)
 2006 (vol 52)
 2005 (vol 51)
 2004 (vol 50)
 2003 (vol 49)