<?xml version='1.0' encoding='UTF-8'?><xml><records><record><source-app name="HighWire" version="7.x">Drupal-HighWire</source-app><ref-type name="Journal Article">17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Buckley, Rita</style></author></authors><secondary-authors><author><style face="normal" font="default" size="100%">Gils, Ann</style></author></secondary-authors></contributors><titles><title><style face="normal" font="default" size="100%">TAFI(a) Assays Measure Extent of Activation in Patient Populations</style></title><secondary-title><style face="normal" font="default" size="100%">MD Conference Express</style></secondary-title></titles><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013-08-01 00:00:00</style></date></pub-dates></dates><pages><style  face="normal" font="default" size="100%">28-29</style></pages><abstract><style  face="normal" font="default" size="100%">Assays for the activated form of thrombin activatable fibrinolysis Inhibitor(a) (TAFIa) can measure the extent of TAFI activation in patient populations. TAFI is a human plasma zymogen that is related to pancreatic carboxypeptidase B (CPB). The active form of TAFI (TAFIa), formed by thrombin cleavage of the zymogen, likely inhibits fibrinolysis by removal of the carboxyl-terminal lysine residues of partially degraded fibrin that stimulate plasminogen activation. TAFI is encoded by the CPB2 gene (chromosome 13) [Boffa MB et al. Biochemistry 1999]. This article presents insights into the function and regulation of TAFI.</style></abstract><number><style face="normal" font="default" size="100%">13</style></number><volume><style face="normal" font="default" size="100%">13</style></volume></record></records></xml>