| pubmed-article:9372107 | pubmed:abstractText | Thrombin generation during coagulation affects the fibrinolysis resistance of clots. This phenomenon is mediated at least in part by a plasma carboxypeptidase that has been called carboxypeptidase-U, carboxypeptidase-R, pro-carboxypeptidase-B, and thrombin-activatable fibrinolysis inhibitor. Carboxypeptidase-U circulates as an inactive proenzyme and is activated by thrombin in a process that is dramatically enhanced by the cofactor thrombomodulin. Clots formed in hemophilic plasma in the presence of a plasminogen activator lyse prematurely and this defect can be correlated by the addition of the missing coagulation factor or thrombomodulin. Thrombin-dependent inhibition of fibrinolysis, which is demonstrable in artificial systems in vitro, may help explain certain in vivo observations, including the delayed bleeding often seen in individuals with hemophilia. | lld:pubmed |
