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Structural and functional characterization of factor XII.

G Tans, J Rosing

    Seminars in Thrombosis and Hemostasis
    |January 1, 1987
    PubMed
    Summary
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    Factor XII (FXII) initiates contact activation on negatively charged surfaces via reciprocal activation with prekallikrein. FXIIa then activates Factor XI, propagating the coagulation cascade.

    Area of Science:

    • Biochemistry
    • Hematology
    • Molecular Biology

    Background:

    • Contact activation is initiated by Factor XII (FXII), a zymogen with a central role in hemostasis.
    • FXII's involvement in initiating and propagating contact activation reactions has been extensively studied.
    • Understanding these molecular events is crucial for comprehending coagulation disorders.

    Purpose of the Study:

    • To review current knowledge on Factor XII's role in contact activation.
    • To summarize the major molecular events in surface-dependent contact activation.
    • To elucidate the reciprocal activation mechanism involving FXII and prekallikrein.

    Main Methods:

    • Literature review of current knowledge on Factor XII and contact activation.
    • Analysis of protein interactions and reaction mechanisms.

    Related Experiment Videos

  • Summary of molecular events in surface-dependent contact activation.

    • Main Results:

    • Factor XII readily binds to negatively charged surfaces.
    • A reciprocal activation mechanism between FXII and prekallikrein is central to FXII activation.
    • Surface-bound FXIIa activates Factor XI, propagating the contact activation pathway.

    Conclusions:

    • Factor XII plays a pivotal role in initiating contact activation through surface binding and reciprocal activation.
    • The reciprocal activation mechanism is the primary driver of FXII activation at surfaces.
    • FXIIa activation is essential for propagating the initial trigger in the contact activation pathway.