New clues regarding the mysterious mechanism of activated thrombin-activatable fibrinolysis inhibitor self-destruction

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Abstract

A new TAFI deletion mutant, constructed by Zhou et al. [1], provides us with new clues on the mysterious mechanism of spontaneous TAFIa self-destruction. Thrombin-Activatable Fibrinolysis Inhibitor (TAFI), also known as procarboxypeptidase U, procarboxypeptidase R and procarboxypeptidase B2, is encoded by the CPB2 gene [2]. TAFI is synthesized in the liver and circulates in plasma as a proenzyme. During coagulation, TAFI is activated by a single proteolytic cleavage at Arg92 that releases the activation peptide from the catalytic domain [3]. This article is protected by copyright. All rights reserved
Original languageEnglish
Pages (from-to)1081-1083
JournalJournal of thrombosis and haemostasis
Volume13
Issue number6
DOIs
Publication statusPublished - 2015

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