EC Number   |
General Information |
Reference  |
|---|
   3.4.21.7 | physiological function |
application of plasmin to primary neurons blocks isoflurane-mediated reduction in dendritic filopodial spines and neuronal apoptosis in vitro |
707135 |
| 3.4.21.7 | physiological function |
microglia-derived plasminogen/plasmin facilitate the production/secretion of TGFbeta3 in astrocytes through both proteinase-activated receptor-1 and the downstream phosphatidylinositol 3-kinase-Akt/protein kinase B signaling cascade |
707930 |
| 3.4.21.7 | physiological function |
Western blot analysis of the endometrial stromal cell culture media reveals that cholesterol sulfate inhibits the conversion by plasmin of matrix metalloproteinase-3 from the precursor form to the active form |
708672 |
| 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 | physiological function |
plasmin is the principal protease in milk. Plasmin, but not cathepsin D, cleavage of osteopontin increases cell adhesion mediated by the alphaVbeta3- or alpha5beta1-integrins. Similar cellular adhesion is mediated by plasmin and thrombin-cleaved osteopontin, plasmin can be a potent regulator of osteopontin activity |
712488 |
| 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 | physiological function |
plasmin is essential in preventing periodontitis in mice |
717069 |
| 3.4.21.7 | physiological function |
plasmin triggers chemotaxis of monocyte-derived dendritic cells through an Akt2-dependent pathway and promotes a T-helper type-1 response. Plasmin requires the annexin A2 heterotetramer for chemotactic signaling. Activation of Akt2 leads to extracellular signal-regulated kinase 1/2 activation and the chemotactic response. Plasmin elicits a time-dependent actin polymerization and triggers rapid activation of Akt and mitogen-activated protein kinases, followed by phosphorylation of the regulatory myosin light chain and chemotaxis. In dendritic cells, plasmin activates exclusively Akt2 via a p38 mitogen-activated protein kinase-dependent pathway, not Akt1 and Akt3. Plasmin-stimulated dendritic cells induce polarization of CD4+ T cells toward the interferon-gamma--producing, proinflammatory Th1 phenotype |
717165 |
| 3.4.21.7 | physiological function |
plasminogen incubated with adherent cells is converted into plasmin for activation by constitutively expressed tPA, i.e. tissue-type plasminogen activator, or uPA, i.e. urokinase-type plasminogen activator. Plasmin formed on the cell membrane then induces a unique response characterized by membrane blebbing and vesiculation. If plasmin formation persists, matrix proteins are then degraded, cells lose their attachments and enter the apoptotic process, characterized by DNA fragmentation and specific ultrastructural features. In plasminogen-treated cells, the nucleus shows chromatin condensation, the cytoplasm is disorganized, contains lysis vesicles and mitochondria become electron-dense |
717216 |
| 3.4.21.7 | physiological function |
plasmin and urokinase-type plasminogen activator are ubiquitous proteases that regulate the extracellular environment. Although neither plasmin nor urokinase-type plasminogen activator exhibits allosteric cooperativity, modeling shows that cooperativity occurs at the system level because of substrate competition |
717386 |
