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      Physiological consequences of loss of plasminogen activator gene function in mice.

      Nature
      Animals, Blood Coagulation, physiology, Embryonic and Fetal Development, Fibrin, Fibrinolysis, genetics, Growth, Longevity, Macrophages, Mice, Mutagenesis, Plasminogen Activators, deficiency, Stem Cells, Thrombosis, etiology, Tissue Plasminogen Activator, Urokinase-Type Plasminogen Activator

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          Abstract

          Indirect evidence suggests a crucial role for the fibrinolytic system and its physiological triggers, tissue-type (t-PA) and urokinase-type (u-PA) plasminogen activator, in many proteolytic processes. Inactivation of the t-PA gene impairs clot lysis and inactivation of the u-PA gene results in occasional fibrin deposition. Mice with combined t-PA and u-PA deficiency suffer extensive spontaneous fibrin deposition, with its associated effects on growth, fertility and survival.

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