A factor IX-deficient mouse model for hemophilia B gene therapy.

نویسندگان

  • L Wang
  • M Zoppè
  • T M Hackeng
  • J H Griffin
  • K F Lee
  • I M Verma
چکیده

We have generated a mouse where the clotting factor IX (FIX) gene has been disrupted by homologous recombination. The FIX nullizygous (-/-) mouse was devoid of factor IX antigen in plasma. Consistent with the bleeding disorder, the factor IX coagulant activities for wild-type (+/+), heterozygous (+/-), and homozygous (-/-) mice were 92%, 53%, and <5%, respectively, in activated partial thromboplastin time assays. Plasma factor IX activity in the deficient mice (-/-) was restored by introducing wild-type murine FIX gene via adenoviral vectors. Thus, these factor IX-deficient mice provide a useful animal model for gene therapy studies of hemophilia B.

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عنوان ژورنال:
  • Proceedings of the National Academy of Sciences of the United States of America

دوره 94 21  شماره 

صفحات  -

تاریخ انتشار 1997