EC Number   |
General Information |
Reference |
|---|
   3.4.21.34 | malfunction |
C1-inhibitor deficiency can lead to uncontrolled enzyme activity, which is a clinically significant cause of hereditary angioedema |
732933 |
| 3.4.21.34 | malfunction |
cerebral hematoma expansion triggered by intracerebral infusion of autologous blood is increased in diabetic rats, and this response is ameliorated by plasma kallikrein inhibition and deficiency, respectively |
718150 |
| 3.4.21.34 | malfunction |
enzyme deficiency has minor effect on the haemostatic capacity of gene-deficient mice |
732928 |
| 3.4.21.34 | malfunction |
enzyme deficiency leads to decreased immune cell trafficking in the course of neuroinflammation |
755272 |
| 3.4.21.34 | malfunction |
plasma prekallikrein-deficient mice have reduced thrombosis risk and plasma kallikrein inhibition is associated with reduced experimental gastroenterocolitis and arthritis in rodents |
753667 |
| 3.4.21.34 | malfunction |
prekallikrein-deficient mice are protected from increased BK-driven vascular leakage in retinal vessels, ferric chloride-triggered arterial thrombosis, and hypotension in anaphylaxis models. Prekallikrein-deficient mice have defective ex vivo plasma clotting that leads to a prolonged activated partial thromboplastin time. Chronic plasma kallikrein deficiency induces vascular alterations that cannot be reverted by short-term normalizing plasma kallikrein levels and provides a thromboprotective activity in addition to reduced contact activation |
731539 |
| 3.4.21.34 | physiological function |
diabetes is associated with increased intrinsic pathway activity, which is mediated in part by plasma kallikrein (PK). PK-mediated activation of the plasminogen cascade is implicated in adipocyte differentiation and adipogenesis during mammary gland involution via activation of plasmin-mediated cleavage of preadipocyte stromal matrix |
732933 |
| 3.4.21.34 | physiological function |
hyperglycemia increases cerebral hematoma expansion by plasma kallikrein-mediated osmotic sensitive inhibition of hemostasis, plasma kallikrein-mediated inhibition of collagen-induced platelet aggregation is enhanced by hyperglycemia |
718150 |
| 3.4.21.34 | physiological function |
plasma kallikrein directly activates G protein-coupled protease-activated receptors (PAR) 1 and 2. Plasma kallikrein stimulates ADAM (a disintegrin and metalloprotease) 17 activity via a PAR1/2 receptor-dependent mechanism, leading sequentially to release of the endogenous ADAM17 substrates, amphiregulin and tumor necrosis factor-alpha, metalloprotease-dependent transactivation of epidermal growth factor receptors, and metalloprotease and epidermal growth factor receptor-dependent ERK1/2 activation |
717809 |
| 3.4.21.34 | physiological function |
plasma kallikrein is the carboxypeptidase/esterase enzyme responsible for tyrosinamide removal from neuropeptide Y |
709045 |
