Lack of TAFI increases brain damage and microparticle generation after thrombolytic therapy in ischemic stroke-Reference-Cited by-同舟云学术

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Lack of TAFI increases brain damage and microparticle generation after thrombolytic therapy in ischemic stroke

Published:2015-08 Issue:2 Volume:136 Page:445-450
ISSN:0049-3848
Container-title:Thrombosis Research
language:en
Short-container-title:Thrombosis Research

Author:

Orbe J.,Alexandru N.,Roncal C.,Belzunce M.,Bibiot P.,Rodriguez J.A.,Meijers J.C.M.,Georgescu A.,Paramo J.A.

Funder

Foundation for Applied Medical Research, University of Navarra (Pamplona, Spain)

ERANET-NEURON Program from Ministerio de Economia y Competitividad

Publisher

Elsevier BV

Subject

Hematology

Reference36 articles.

1. Characterization of mouse thrombin-activatable fibrinolysis inhibitor;Marx;Thromb. Haemost.,2000

2. Thrombin-activatable fibrinolysis inhibitor (TAFI, plasma procarboxypeptidase B, procarboxypeptidase R, procarboxypeptidase U);Bouma;J. Thromb. Haemost.,2003

3. The intrinsic threshold of the fibrinolytic system is modulated by basic carboxypeptidases, but the magnitude of the antifibrinolytic effect of activated thrombin-activable fibrinolysis inhibitor is masked by its instability;Walker;J. Biol. Chem.,2004

4. New insights into factors affecting clot stability: A role for thrombin activatable fibrinolysis inhibitor (TAFI; plasma procarboxypeptidase B, plasma procarboxypeptidase U, procarboxypeptidase R);Bouma;Semin. Hematol.,2004

5. Carboxypeptidase U (TAFIa): a new drug target for fibrinolytic therapy?;Willemse;J. Thromb. Haemost.,2009

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