EC Number   |
General Information  |
Reference |
|---|
   3.4.21.7 | malfunction |
Defects or mutations in the PLG gene are the cause of thrombophilia, a form of recurrent thrombosis, and type I plasminogen deficiency. Ligneous conjunctivitis is usually the most common and initial form of type I plasminogen deficiency and is a rare form of chronic conjunctivitis characterized by chronic tearing and redness of the conjunctivae |
717469 |
| 3.4.21.7 | malfunction |
in plasminogen activator inhibotr-1 knock-out mouse embryonic fibroblasts plasmin activity. Unregulated plasmin activity is only partially responsible for TGF-beta activation as evidenced by a mere 25% reduction in TGF-beta activity when plasmin is inhibited |
709033 |
| 3.4.21.7 | malfunction |
in plasminogen-deficient mice, periodontitis progresses rapidly, within 20 weeks. The plasminogen-deficient mice show detachment of gingival tissue, resorption of the cementum layer, formation of necrotic tissue, and severe alveolar bone degradation, phenotype, overview. Supplementation by injection of plasminogen-deficient mice with human plasminogen for 10 days leads to necrotic tissue absorption, inflammation subsidence, and full regeneration of gum tissues |
717069 |
| 3.4.21.7 | malfunction |
plasmin inhibition by tranexamic acid upregulates the profibrogenic genes, which respond to TGF-beta-intracellular signalling |
718070 |
| 3.4.21.7 | malfunction |
the plasminogen activation system is impaired in idiopathic pulmonary fibrosis |
-, 717845 |
| 3.4.21.7 | metabolism |
besides the main physiological inhibitor alpha2-antiplasmin, the plasmin-antiplasmin system is also regulated by the general protease inhibitor alpha2-macroglobulin, a member of the protease inhibitor I39 family. The activity of the plasminogen activators is primarily regulated by the plasminogen activator inhibitors 1 and 2, members of the serine protease inhibitor superfamily |
717469 |
| 3.4.21.7 | more |
overexpression of human urokinase plasminogen activator in HSC 180 cells leads to increased plasmin activity, which is blocked by tranexamic acid in the transduced. Plasmin overexpression in the transduced cells significantly decreases gene expression of profibrogenic molecules, i.e. a1(I)collagen by 66%, TIMP-1 by 59%, alpha-smooth muscle actin by 90%, and TGF-beta by 55%. Both SnoN gene and protein expression increased prominently |
718070 |
| 3.4.21.7 | more |
pasteurization of whey protein-free retentate of micro- and difiltrated milk at 95°C for 15 s does not significantly affect plasmin or plasminogen-derived activities. The retentate contains increased plasmin activity, proportional to the concentration of beta-lactoglobulin |
717666 |
| 3.4.21.7 | more |
plasminogen activation to plasmin restores lipid mediator prostaglandin E2 sensitivity in fibrotic lung fibroblasts involving amplified protein kinase A signaling resulting from the promotion of new interactions between AKAP9 and protein kinase A regulatory subunit II in the perinuclear region as well as from the inhibition of protein phosphatase 2A |
-, 717845 |
| 3.4.21.7 | more |
plasminogen is a major surface-bound protein interacting with pathogen Bacillus anthracis, it efficiently binds to spores of Bacillus anthracis in a lysine- and exosporium-dependent manner with alpha-enolase and elongation factor as specific receptors. Plasminogen-bound spores are capable of exhibiting anti-opsonic properties by cleaving C3b molecules in vitro and in rabbit bronchoalveolar lavage fluid, resulting in a decrease in macrophage phagocytosis. Mechanisms involved in the evasion of innate immunity by Bacillus anthracis through recruitment of plasminogen resulting in the enhancement of anti-complement and anti-opsonization properties of the pathogen, overview |
718277 |
