Thromb Haemost 2007; 98(03): 530-542
DOI: 10.1160/TH07-02-0150
Theme Issue Article
Schattauer GmbH

Coagulation factor V and thrombophilia: Background and mechanisms

Kenneth Segers
1  Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands
,
Björn Dahlbäck
2  Department of Laboratory Medicine, Clinical Chemistry, Lund University, Wallenberg Laboratory, University Hospital, Malmö, Sweden
,
Gerry A. F. Nicolaes
1  Department of Biochemistry, Cardiovascular Research Institute Maastricht, Maastricht University, Maastricht, The Netherlands
› Author Affiliations
Financial support:This work was supported by VIDI grant no. 916–046–330 from the Netherlands Organization for Scientific Research (N.W.O. to G.A.F.N.).
Further Information

Publication History

Received 27 February 2007

Accepted after revision 17 April 2007

Publication Date:
28 November 2017 (online)

Summary

Human coagulation factor V (FV) is an essential coagulation protein with functions in both the pro- and anticoagulant pathways. Failure to express and control FV functions can either lead to bleeding, or to thromboembolic disease. Both events may develop into a life-threatening condition. Since the first description of APC resistance, and in particular the description of the so-called factor VLeiden mutation, in which a prominent activated protein C cleavage site in FV has been abolished through a mutation in the FV gene, FV has been in the center of attention of thrombosis research. In this review we describe how the functions of FV are expressed and regulated and provide an extensive description of the role that FV plays in the etiology of thromboembolic disease.