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	additional information	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	additional information	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	additional information	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	additional information	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	
3.4.21.7	additional information	released from CORM-2 and nitric oxide via a NO donor to induce carboxyheme and metheme states, respectively. CO elicits hypofibrinolysis by enhancing alpha2-antiplasmin activity and decreasing plasmin activity	717417	
3.4.21.7	additional information	the catalytic triad is formed by His603, Asp646, and Ser741	717469	
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	contribution of plasmin to amplification of inflammation in patients with psoriasis. Annexin II, a receptor for plasmin is dramatically increased in both dermis and epidermis in psoriasis. Plasmin at sites of inflammation is pro-inflammatory, eliciting production of inflammatory factors, including CC chemokine ligand 20 and interleukin-23, that is mediated by the nuclear factor-kappaB (NF-kB) signaling pathway and that has an essential role in the recruitment and activation of pathogenic C-C chemokine receptor type 6+ T cells	718272	
3.4.21.7	physiological function	inactivation of ADAMTS13 by plasmin as a potential cause of thrombotic thrombocytopenic purpura, propagation by deficiency of alpha2-antiplasmin function in acute-phase, but not remission-phase plasma, overview. ADAMTS13 is truncated at the C-terminus during the acute phase	718043	
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	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	
3.4.21.7	physiological function	plasmin cleavage of inactive complement component C3b regulates macrophage interleukin-12 secretion	732405	
3.4.21.7	physiological function	plasmin is essential in preventing periodontitis in mice	717069	
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	physiological function	plasmin plays a key role in the regulation of profibrogenic molecules in hepatic stellate cells, role of plasmin in profibrogenic molecule expression, SnoN transcriptional kinetics and gelatinase activation	718070	
3.4.21.7	physiological function	plasmin stimulates phosphorylation of ERK1/2 and p38 MAPK. Plasminogen/plasmin modulates bone metabolism by regulating the osteoblast and osteoclast function. Exogenous plasmin clearly induces the osteoprotegerin expression in plasminogen-deficient osteoblasts. Plasmin activates JNK, but the inhibition of JNK does not attenuate plasmin-induced osteoprotegerin expression	717866	
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	plasmin, converted from plasminogen by plasminogen activators, plays an essential role in amplification of psoriasiform skin inflammation in mice. Intradermal injection of plasmin or plasmin together with recombinant monocyte/macrophage chemotactic protein-1 results in induction of psoriasiform skin inflammation around the injection sites in mice. Histological analysis of skin sections from mice treated with plasmin and rMCP-1 reveal acanthosis, hyperorthokeratosis, subcorneal microabscesses, dilated lymphatic vessels and a diffuse inflammatory infiltrates in the dermis compared to normal epidermis and dermis in the ears of control mice. Plasmin triggers NF-kB-dependent IL-23 and CCL20 expression in macrophages	718272	
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	primary function of plasmin is the cleavage of insoluble fibrin polymers at specific sites resulting in soluble fragments. In addition, plasmin acts as a proteolytic factor in many other physiological processes such as mediation of cell migration by degrading the extracellular matrix, wound healing, tissue remodelling, angiogenesis, embryogenesis, and pathogen and tumour cell invasion. The plasmin-antiplasmin system plays a key role in blood coagulation and fibrinolysis. Plasmin and alpha2-antiplasmin are primarily responsible for a controlled and regulated dissolution of the fibrin polymers into soluble fragments	717469	
3.4.21.7	physiological function	proteolytic activation of ENaC by plasmin contributes to Na+ retention and hypertension in preeclampsia	731900	
3.4.21.7	physiological function	the plasminogen activation system, in which plasminogen is cleaved to plasmin, comprises an anti-fibrotic pathway that both suppresses the development of pulmonary fibrosis in vivo	-, 717845	
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