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The Nijmegen Hemostasis Assay: Simultaneous Fluorogenic Measurement of Thrombin and Plasmin Generation in a Single Well
Published on: February 27, 2026
106
Coagulation factor XIIIa is inactivated by plasmin
Woosuk S Hur1, Nima Mazinani1, X J David Lu1
1Michael Smith Laboratories and Department of Biochemistry and Molecular Biology, University of British Columbia, Vancouver, BC, Canada; and.
Blood
|September 12, 2015
Summary
Plasmin inactivates coagulation factor XIIIa (FXIIIa), an enzyme crucial for stabilizing blood clots. This finding reveals a new mechanism for regulating blood clot stability and FXIIIa activity.
Area of Science:
- Biochemistry
- Hematology
- Molecular Biology
Background:
- Coagulation factor XIIIa (FXIIIa) stabilizes blood clots by cross-linking proteins.
- The physiological inactivation mechanism of FXIIIa has not been clearly defined.
Purpose of the Study:
- To investigate the interaction between plasmin and FXIIIa.
- To elucidate the mechanism of FXIIIa inactivation in physiological conditions.
Main Methods:
- Mass spectrometry was used to identify cleavage sites.
- In vitro assays were performed using purified FXIIIa and plasmin.
- Experiments were conducted in plasma deficient in fibrinogen and in plasma treated with tissue plasminogen activator.
Main Results:
- Plasmin rapidly cleaves and inactivates FXIIIa with a catalytic efficiency of 8.3 × 10(3) M(-1)s(-1).
- The primary cleavage site was identified between K468 and Q469.
- Both plasma- and platelet-derived FXIIIa are susceptible to plasmin-mediated degradation.
- FXIIIa inactivation occurs during clot lysis and is enhanced in specific plasma conditions.
Conclusions:
- Plasmin is a physiological enzyme that inactivates FXIIIa.
- Fibrinolytic activity can modulate FXIIIa function, impacting blood protein cross-linking.
- This study uncovers a novel regulatory pathway for blood clot stability.
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