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Association between genetic variation at the ADAMTS13 locus and ischemic stroke
Author(s) -
HANSON E.,
JOOD K.,
NILSSON S.,
BLOMSTRAND C.,
JERN C.
Publication year - 2009
Publication title -
journal of thrombosis and haemostasis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.947
H-Index - 178
eISSN - 1538-7836
pISSN - 1538-7933
DOI - 10.1111/j.1538-7836.2009.03617.x
Subject(s) - ischemic stroke , locus (genetics) , genetic variation , genome wide association study , medicine , genetic association , adamts13 , variation (astronomy) , genetics , biology , genotype , gene , single nucleotide polymorphism , ischemia , von willebrand factor , platelet , physics , astrophysics
von Willebrand factor (VWF) is a large glycoprotein involved in the early stages of hemostasis, where it recruits platelets to sites of vessel injury [1]. Plasma VWF is composed of multimers. The biological activity of VWF is related to the size of these multimers, with the larger ones being more hemostatically effective than the smaller forms [2]. VWF multimeric size is modulated by ADAMTS13 (a disintegrin and metalloprotease with thrombospondin motif) [2]. Decreased plasma levels of ADAMTS13 have been reported in patients with myocardial infarction, both acutely [3] and several months after the event [4]. In a recent study on arterial thrombosis at young age, Bongers et al. observed a reduction in plasma levels of ADAMTS13 antigen and activity 1– 3 months after the event in patients with coronary heart disease [5].