Clinical Chemistry
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Clinical Chemistry 52: 30-36, 2006. First published November 18, 2005; 10.1373/clinchem.2005.055814
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
clinchem.2005.055814v1
52/1/30    most recent
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (16)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Willemse, J. L.
Right arrow Articles by Hendriks, D. F.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Willemse, J. L.
Right arrow Articles by Hendriks, D. F.
Related Collections
Right arrow Hemostasis and Thrombosis
(Clinical Chemistry. 2006;52:30-36.)
© 2006 American Association for Clinical Chemistry, Inc.

Minireviews

Measurement of Procarboxypeptidase U (TAFI) in Human Plasma: A Laboratory Challenge

Johan L. Willemse and Dirk F. Hendriksa

Laboratory of Medical Biochemistry, University of Antwerp, B-2610 Wilrijk, Belgium.

aAuthor for correspondence. Fax 32-3820-2745; e-mail dirk.hendriks{at}ua.ac.be.


Abstract

Background: The importance of carboxypeptidase U (CPU) as a novel regulator of the fibrinolytic rate has attracted much interest during recent years. CPU circulates in plasma as a zymogen, proCPU, that can be activated by thrombin, thrombin-thrombomodulin (T-Tm), or plasmin. Given that the proCPU concentration in plasma is far below its Km for activation by the T-Tm complex, the formation of CPU will be directly proportional to the proCPU concentration. A low or high proCPU plasma concentration might therefore tip the balance between profibrinolytic and antifibrinolytic pathways and thereby cause a predisposition to bleeding or thrombosis.

Content: To measure plasma proCPU concentrations, different methods have been developed based on 2 different principles: antigen determination and measurement of CPU activity after quantitative conversion of the proenzyme to its active form by addition of T-Tm. The major drawbacks that should be kept in mind when analyzing clinical samples by both principles are reviewed.

Conclusions: proCPU is a potential prothrombotic risk factor. Evaluation of its relationship with thrombosis requires accurate assays. Many assays used in different clinical settings are inadequately validated, forcing reconsideration of conclusions made in these reports.




The following articles in journals at HighWire Press have cited this article:


Home page
 BloodHome page
M. B. Boffa, D. Maret, J. D. Hamill, N. Bastajian, P. Crainich, N. S. Jenny, Z. Tang, E. M. Macy, R. P. Tracy, R. F. Franco, et al.
Effect of single nucleotide polymorphisms on expression of the gene encoding thrombin-activatable fibrinolysis inhibitor: a functional analysis
Blood, January 1, 2008; 111(1): 183 - 189.
[Abstract] [Full Text] [PDF]

Home page
 BloodHome page
T. M. Binette, F. B. Taylor Jr, G. Peer, and L. Bajzar
Thrombin-thrombomodulin connects coagulation and fibrinolysis: more than an in vitro phenomenon
Blood, November 1, 2007; 110(9): 3168 - 3175.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2006 by the American Association for Clinical Chemistry.