EC Number   |
Application |
Reference |
|---|
   3.4.21.B1 | analysis |
substrate Ala-Lys-Nle-Arg-7-amido-4-methylcoumarin can be used to measure FSAP activity in plasma |
755578 |
| 3.4.21.B1 | medicine |
FSAP accumulation in coronary atherosclerotic lesions, is due to either local synthesis by monocytes/macrophages, or uptake from the plasma due to plaque hemorrhage. Higher expression of FSAP in unstable plaques may destabilize plaque through reducing vascular smooth muscle cell proliferation/migration and altering the hemostatic balance |
684801 |
| 3.4.21.B1 | medicine |
FSAP measures are higher in women compared with age-matched men. The extent of coronary artery calcification in women is positively associated with total FSAP, but negatively associated with the specific activity of FSAP. No difference in FSAP measures is observed in men |
753075 |
| 3.4.21.B1 | medicine |
FSAP-alpha2-antiplasmin complex levels are markedly elevated in patients with Gram-negative sepsis as compared with controls. The FSAP level increases by 16.82 AU/ml in patients with melioidosis after adjustment for the effect of diabetes melitus in the regression model. FSAP activation is correlated with nucleosome release. No difference in FSAP activation on admission is seen between survivors and non-survivors, but the extent of FSAP activation correlates with stage of the disease |
754512 |
| 3.4.21.B1 | medicine |
HABP2 is an important regulator of lung cancer progression. HABP2 expression is increased in several subtypes of patient non-small cell lung cancer samples. 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 | medicine |
plays a role in physiologic function of the pericellular environment of the vasculature. Proteolytically inactivates growth factors. May regulate angiogenic processes, like neovascularisation during tissue remodelling, wound repair or tumor progression. May contribute to extravascular fibrin deposition and inflammatory processes in the injured lung |
687108 |
| 3.4.21.B1 | medicine |
proangiogenic potential of HABP, which, in combination with a profibrinolytic activity, directs the physiological function of this plasma protease to processes in which clot lysis, cell motility and neovascularisation are pivotal processes, e.g., in wound healing, tissue repair and tumour progession |
685438 |
| 3.4.21.B1 | medicine |
role in atherosclerosis, contributes to vascular fibroproliferative inflammatory diseases in the context of pericellular proteolysis of the extracellular matrix, growth factor activity and haemostasis |
690121 |
| 3.4.21.B1 | medicine |
the G534E variant of FSAP is a risk locus for chronic hepatitis C virus(HCV)-induced liver fibrosis and cirrhosis by determining platelet-derived growth factor BB (PDGF-BB)mediated hepatic stellate cell proliferation through a single amino acid substitution in FSAP. FSAP G534E might be useful for risk stratification in patients with HCV infection |
692559 |
| 3.4.21.B1 | more |
nucleic acids are cofactors for FSAP-mediated inhibition of platelet-derived growth factor-BB-induced cell proliferation and mitogen-activated protein kinase 44/42 phosphorylation in vascular smooth muscle cells. FSAP protects RNA from the actions of RNase |
684975 |
