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.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Animals
-
Blood Coagulation / physiology
-
Embryonic and Fetal Development / physiology
-
Fibrin / physiology
-
Fibrinolysis / genetics
-
Fibrinolysis / physiology*
-
Growth / genetics
-
Growth / physiology
-
Longevity / genetics
-
Longevity / physiology
-
Macrophages / physiology
-
Mice
-
Mutagenesis
-
Plasminogen Activators / deficiency
-
Plasminogen Activators / genetics
-
Plasminogen Activators / physiology*
-
Stem Cells
-
Thrombosis / etiology
-
Tissue Plasminogen Activator / deficiency
-
Tissue Plasminogen Activator / genetics
-
Tissue Plasminogen Activator / physiology
-
Urokinase-Type Plasminogen Activator / deficiency
-
Urokinase-Type Plasminogen Activator / genetics
-
Urokinase-Type Plasminogen Activator / physiology
Substances
-
Fibrin
-
Plasminogen Activators
-
Tissue Plasminogen Activator
-
Urokinase-Type Plasminogen Activator