Thrombosis from a prothrombin mutation conveying antithrombin resistance.

نویسندگان

  • 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
چکیده

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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عنوان ژورنال:
  • The New England journal of medicine

دوره 366 25  شماره 

صفحات  -

تاریخ انتشار 2012