EC Number   |
General Information |
Reference |
|---|
   3.4.21.B1 | evolution |
the active site residues of a serine proteinase are conserved in the serine protease domain of the enzyme. The enzyme has a similar domain structure and tissue distribution to those of human hyaluronan binding protein 2 (HABP2), putative phylogenetic tree |
731684 |
| 3.4.21.B1 | malfunction |
the variant Marburg I polymorphism results in low enzymatic activity and is associated with an enhanced risk of carotid stenosis and stroke |
717169 |
| 3.4.21.B1 | metabolism |
FSAP is exclusively activated by the positively charged surfaces polyethylenimine and poly-L-lysine, not by the negatively charged glass or self-assembled monolayer with carboxyl group termination or uncharged (Teflon AF) surfaces. Activation is concomitant with coagulation. A contact phase inhibitor diminishes coagulation to background levels for all surfaces except polyethylenimine |
752346 |
| 3.4.21.B1 | physiological function |
factor VII-activating protease has potential effects on hemostasis |
718425 |
| 3.4.21.B1 | physiological function |
FSAP alters fibrin clot properties by fibrinogenolysis. Treatment of human fibrinogen with FSAP releases truncated fibrinogen which shows a delayed thrombin-catalyzed polymerization and forms fibrin clots of reduced turbidity. The clots reveal a less coarse fibrin network with thinner fibers and a smaller pore size. FSAP-treated fibrinogen or plasma exhibits a significantly faster tissue plasminogen activator-driven lysis, which correlates exclusively with cleavage of fibrinogen and not with activation of plasminogen activators |
752838 |
| 3.4.21.B1 | physiological function |
HABP2 overexpression increases LMW-HA-induced urokinase plasminogen activator activation, migration, and extravasation in human lung adenocarcinoma cells. In vivo, overexpression of HABP2 in human lung adenocarcinoma cells increases primary tumor growth rates in nude mice by about 2fold and lung metastasis by about 10fold compared to vector control cells |
753699 |
| 3.4.21.B1 | physiological function |
phorbol ester-mediated neutrophil extracellular trap (NET) formation is marginally stimulated by FSAP. Plasma-derived FSAP as well as exogenous FSAP binds to NET, and FSAP and NETs colocalize in coronary thrombi from patients with acute myocardial infarction. No activation of pro-FSAP by NETs is evident, but after disintegration of NETs with DNase, a robust activation of pro-FSAP, due to release of histones from nucleosomes, is detected. The released histones are in turn degraded by FSAP. Histone cytotoxicity towards endothelial cells is neutralized by FSAP more potently than by activated protein C |
755588 |
| 3.4.21.B1 | physiological function |
the enzyme plays roles in regulating inflammation, vascular function, fibrosis and atherosclerosis |
717319 |
| 3.4.21.B1 | physiological function |
the enzyme regulates hemostasis- and remodeling-associated processes in the vasculature |
717169 |
| 3.4.21.B1 | physiological function |
the serine protease is possibly involved in the extracellular matrix turnover. It might be involved in the post-mortem fish muscle softening |
731684 |
