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Gene targeting in hemostasis. factor XI.

D Gailani1

  • 1Departments of Pathology and Medicine, Vanderbilt University, Nashville, TN, USA. Dave.Gailani@mcmail.vanderbilt.edu

Frontiers in Bioscience : a Journal and Virtual Library
|February 15, 2001
PubMed
Summary

Factor XI (FXI) deficiency causes variable bleeding but not spontaneous hemorrhage. FXI deficiency partially mitigates severe protein C deficiency-related hypercoagulability, indicating a role in thrombosis.

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Area of Science:

  • Coagulation cascade
  • Hemostasis and thrombosis research

Background:

  • Factor XI (FXI) is a plasma serine protease zymogen crucial for activating factor IX (FIX).
  • FXI supports thrombin generation for fibrin clot consolidation and resistance to fibrinolysis.
  • Congenital FXI deficiency in humans leads to variable bleeding but not spontaneous hemorrhage like hemophilia.

Purpose of the Study:

  • To investigate the hemostatic role of Factor XI (FXI).
  • To evaluate the impact of FXI deficiency on thrombotic conditions.

Main Methods:

  • Analysis of FXI-/- mice for hemostatic deficits.
  • Cross-breeding FXI-/- mice with protein C deficient mice.

Main Results:

  • FXI-/- mice exhibited prolonged activated partial thromboplastin times but no spontaneous hemorrhage.
  • Tail bleeding assays showed only slight, inconsistent bleeding prolongation in FXI-/- mice.
  • Severe FXI deficiency partially ameliorated hypercoagulability in protein C deficient mice.

Conclusions:

  • Factor XI plays a limited role in hemostasis, primarily in sustaining thrombin production.
  • Factor XI contributes to thrombotic conditions, as evidenced by its role in protein C deficiency-induced hypercoagulability.

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