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Anticoagulant Drugs: Low-Molecular-Weight Heparins

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Related Experiment Video

Updated: May 27, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

Published on: September 9, 2012

The anticoagulant function of coagulation factor V.

Thomas J Cramer¹, Andrew J Gale

¹Department of Molecular and Experimental Medicine, The Scripps Research Institute, 10550 North Torrey Pines Road, La Jolla, CA 92037, USA.

Thrombosis and Haemostasis

|November 26, 2011

Summary

Factor V (FV) acts as an anticoagulant cofactor for activated protein C (APC). The FV(Leiden) mutation impairs this function, increasing thrombotic risk by reducing APC cofactor activity and FVa inactivation.

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Last Updated: May 27, 2026

Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay

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Published on: September 9, 2012

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Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)

Determination of the Procoagulant Activity of Extracellular Vesicle (EV) Using EV-Activated Clotting Time (EV-ACT)

Published on: August 4, 2023

Area of Science:

Biochemistry
Hematology
Molecular Biology

Background:

The anticoagulant function of factor V (FV) as a cofactor for activated protein C (APC) was discovered nearly two decades ago.
The FV(Leiden) mutation (R506Q) impairs APC-mediated inactivation of FV and FVIIIa, increasing thrombotic risk.
FV(Leiden) is prevalent in Caucasian populations, highlighting its clinical significance.

Purpose of the Study:

To elucidate the mechanistic and structural properties of FV's anticoagulant function.
To understand how FV(Leiden) mutation affects FV's anticoagulant cofactor activity.
To investigate the requirements for FV's anticoagulant function.

Main Methods:

Characterization of FV anticoagulant function through biochemical assays.
Analysis of FV cleavage at position 506 by APC.
Investigation of the role of FV domains (B domain, A3 domain) and cofactors (Protein S) in FV anticoagulant activity.

Main Results:

APC cleavage at FV position 506 is essential for anticoagulant function.
The FV B domain's C-terminal part and its connection to the A3 domain are critical.
FV requires binding to negatively charged phospholipid membranes and the presence of Protein S.
FV serves as a cofactor for the inactivation of both FVa and FVIIIa by APC.
FV(Leiden)'s prothrombotic effect stems from reduced APC cofactor activity and FVa resistance to APC.

Conclusions:

FV's anticoagulant function is a complex process involving specific structural features, cofactor interactions, and membrane binding.
The FV(Leiden) mutation disrupts these mechanisms, leading to a prothrombotic state.
Further research is needed to fully explore the detailed structural and mechanistic properties of FV's anticoagulant role.