Thrombosis from a Prothrombin Mutation Conveying Antithrombin Resistance
Author(s) -
Yuhri Miyawaki,
Atsuo Suzuki,
Junko Fujita,
Asuka Maki,
Eriko Okuyama,
Moe Murata,
Akira Takagi,
Takashi Murate,
Shinji Kunishima,
Michio Sakai,
Kohji Okamoto,
Tadashi Matsushita,
Tomoki Naoe,
Hidehiko Saito,
Tetsuhito Kojima
Publication year - 2012
Publication title -
new england journal of medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 19.889
H-Index - 1030
eISSN - 1533-4406
pISSN - 0028-4793
DOI - 10.1056/nejmoa1201994
Subject(s) - antithrombin , thrombin , medicine , mutation , mutant , arginine , thrombosis , endocrinology , biochemistry , gene , chemistry , platelet , heparin , amino acid
We identified a novel mechanism of hereditary thrombosis associated with antithrombin resistance, with a substitution of arginine for leucine at position 596 (p.Arg596Leu) in the gene encoding prothrombin (called prothrombin Yukuhashi). The mutant prothrombin had moderately lower activity than wild-type prothrombin in clotting assays, but the formation of thrombin-antithrombin complex was substantially impaired. A thrombin-generation assay revealed that the peak activity of the mutant prothrombin was fairly low, but its inactivation was extremely slow in reconstituted plasma. The Leu596 substitution caused a gain-of-function mutation in the prothrombin gene, resulting in resistance to antithrombin and susceptibility to thrombosis.
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