By A. Bulikova
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Additional resources for Antiphospholipid Syndrome
48, 719-721. Schwarzenbacher R, Zeth K, Diederichs K, Gries A, Kostner GM, Laggner P & Prassl R. (1999) Crystal structure of human beta2-glycoprotein I: implications for phospholipid binding and the antiphospholipid syndrome. EMBO J. 18(22), 62286239. Seshan SV, Franzke CW, Redecha P, Monestier M, Mackman N & Girardi G. (2009) Role of tissue factor in a mouse model of thrombotic microangiopathy induced by antiphospholipid antibodies. Blood. 114(8), 1675-1683. Urbanus RT, Pennings MT, Derksen RH & de Groot PG.
2010). Blood contains microparticles (MPs) derived from a variety of cell types, including platelets, monocytes, and endothelial cells. MPs are formed from membrane blebs that are released from the cell surface by proteolytic cleavage of the cytoskeleton (Owens & Mackman, 2011). MPs may be procoagulant because they provide a membrane surface for the assembly of components of the coagulation protease cascade. Importantly, 30 Antiphospholipid Syndrome procoagulant activity is increased by the presence of anionic phospholipids, particularly phosphatidylserine (PS), and the procoagulant protein tissue factor (TF), which is the major cellular activator of the clotting cascade (Owens & Mackman, 2011).
Beta(2)-glycoprotein I deficiency: prevalence, genetic background and effects on plasma lipoprotein metabolism and hemostasis. Atherosclerosis 152:337-346. A. 2004. Beta-2 glycoprotein I and its role in antiphospholipid syndrome-lessons from knockout mice. Clin Immunol 112:136-143.  Cleve, H. 1968. [Genetic studies on the deficiency of beta 2-glycoprotein I of human serum]. Humangenetik 5:294-304. M. 1992. Beta 2-glycoprotein I deficiency and the risk of thrombosis. Thromb Haemost 67:649-653.