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Literature summary extracted from

  • Korhonen, T.K.
    Fibrinolytic and procoagulant activities of Yersinia pestis and Salmonella enterica (2015), J. Thromb. Haemost., 13 Suppl 1, S115-S120 .
    View publication on PubMed

Natural Substrates/ Products (Substrates)

EC Number Natural Substrates Organism Comment (Nat. Sub.) Natural Products Comment (Nat. Pro.) Rev. Reac.
3.4.23.48 alpha2-antiplasmin + H2O Yersinia pestis alpha2AP is the main inhibitor of free plasmin in the circulation. Pla cleaves and inactivates alpha2AP by a single, rapid cut. It appears likely that the R376-M377 bait peptide bond is targeted by Pla ?
-
 ?
3.4.23.48 plasminogen + H2O Yersinia pestis activation plasmin + ?
-
 ?
3.4.23.48 plasminogen activator inhibitor-1 + H2O Yersinia pestis inactivation. PAI-1 is the primary physiological inhibitor of uPA and t-PA and a major inhibitor of fibrinolysis. Pla rapidly inactivates PAI-1 by a single cleavage of the bait peptide at R346-M347. In circulation, most PAI-1 is bound to vitronectin, which is also degraded by Pla ?
-
 ?
3.4.23.48 single-chain urokinase + H2O Yersinia pestis activation ?
-
 ?
3.4.23.48 TAFI + H2O Yersinia pestis TAFI is secreted into plasma as a procarboxypeptidase, it is a regulatory protein linking the coagulation and fibrinolytic systems, and TAFI is protective in septic yersionosis. Pla cleaves at the C-terminal region of TAFI and reduces its activation to TAFIa TAFIa + ?
-
 ?
3.4.23.48 tissue factor pathway inhibitor + H2O Yersinia pestis TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme Pla cleaves the tissue factor pathway inhibitor, TFPI ?
-
 ?
3.4.23.49 alpha2-antiplasmin + H2O Salmonella enterica subsp. enterica serovar Typhimurium inactivation ?
-
 ?
3.4.23.49 factor B + H2O Salmonella enterica subsp. enterica serovar Typhimurium
-
 ?
-
 ?
3.4.23.49 factor H + H2O Salmonella enterica subsp. enterica serovar Typhimurium
-
 ?
-
 ?
3.4.23.49 gelatine + H2O Salmonella enterica subsp. enterica serovar Typhimurium degradation ?
-
 ?
3.4.23.49 plasminogen + H2O Salmonella enterica subsp. enterica serovar Typhimurium activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin. PgtE addresses the control systems rather than direct plasminogen activation plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin. PgtE addresses the control systems rather than direct plasminogen activation plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin. PgtE addresses the control systems rather than direct plasminogen activation plasmin + ?
-
 ?
3.4.23.49 plasminogen activator inhibitor-1 + H2O Salmonella enterica subsp. enterica serovar Typhimurium inactivation ?
-
 ?
3.4.23.49 TAFI + H2O Salmonella enterica subsp. enterica serovar Typhimurium TAFI is secreted into plasma as a procarboxypeptidase, it is a regulatory protein linking the coagulation and fibrinolytic systems, and TAFI is protective in septic yersionosis. PptE cleaves at the C-terminal region of TAFI and reduces its activation to TAFIa TAFIa + ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O Salmonella enterica subsp. enterica serovar Typhimurium TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme PgtE cleaves the tissue factor pathway inhibitor, TFPI ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme PgtE cleaves the tissue factor pathway inhibitor, TFPI ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme PgtE cleaves the tissue factor pathway inhibitor, TFPI ?
-
 ?

Organism

EC Number Organism UniProt Comment Textmining
3.4.23.48 Yersinia pestis P17811
-
-
3.4.23.49 Salmonella enterica subsp. enterica serovar Typhimurium P06185
-
-
3.4.23.49 Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 P06185
-
-
3.4.23.49 Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 P06185
-
-

Substrates and Products (Substrate)

EC Number Substrates Comment Substrates Organism Products Comment (Products) Rev. Reac.
3.4.23.48 alpha2-antiplasmin + H2O inactivation Yersinia pestis ?
-
 ?
3.4.23.48 alpha2-antiplasmin + H2O alpha2AP is the main inhibitor of free plasmin in the circulation. Pla cleaves and inactivates alpha2AP by a single, rapid cut. It appears likely that the R376-M377 bait peptide bond is targeted by Pla Yersinia pestis ?
-
 ?
3.4.23.48 plasminogen + H2O activation Yersinia pestis plasmin + ?
-
 ?
3.4.23.48 plasminogen activator inhibitor-1 + H2O inactivation Yersinia pestis ?
-
 ?
3.4.23.48 plasminogen activator inhibitor-1 + H2O inactivation. PAI-1 is the primary physiological inhibitor of uPA and t-PA and a major inhibitor of fibrinolysis. Pla rapidly inactivates PAI-1 by a single cleavage of the bait peptide at R346-M347. In circulation, most PAI-1 is bound to vitronectin, which is also degraded by Pla Yersinia pestis ?
-
 ?
3.4.23.48 single-chain urokinase + H2O activation Yersinia pestis ?
-
 ?
3.4.23.48 TAFI + H2O inactivation Yersinia pestis TAFIa + ?
-
 ?
3.4.23.48 TAFI + H2O TAFI is secreted into plasma as a procarboxypeptidase, it is a regulatory protein linking the coagulation and fibrinolytic systems, and TAFI is protective in septic yersionosis. Pla cleaves at the C-terminal region of TAFI and reduces its activation to TAFIa Yersinia pestis TAFIa + ?
-
 ?
3.4.23.48 tissue factor pathway inhibitor + H2O inactivation Yersinia pestis ?
-
 ?
3.4.23.48 tissue factor pathway inhibitor + H2O TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme Pla cleaves the tissue factor pathway inhibitor, TFPI Yersinia pestis ?
-
 ?
3.4.23.49 alpha2-antiplasmin + H2O inactivation Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 factor B + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 factor H + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 Gelatin + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 Gelatin + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 ?
-
 ?
3.4.23.49 Gelatin + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 ?
-
 ?
3.4.23.49 gelatine + H2O degradation Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 plasminogen + H2O activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin. PgtE addresses the control systems rather than direct plasminogen activation Salmonella enterica subsp. enterica serovar Typhimurium plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin Salmonella enterica subsp. enterica serovar Typhimurium plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin. PgtE addresses the control systems rather than direct plasminogen activation Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin. PgtE addresses the control systems rather than direct plasminogen activation Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 plasmin + ?
-
 ?
3.4.23.49 plasminogen + H2O activation, but PgtE does not catalyze formation of stable plasmin activity because it cleaves also the B chain of plasmin Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 plasmin + ?
-
 ?
3.4.23.49 plasminogen activator inhibitor-1 + H2O inactivation Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 TAFI + H2O TAFI is secreted into plasma as a procarboxypeptidase, it is a regulatory protein linking the coagulation and fibrinolytic systems, and TAFI is protective in septic yersionosis. PptE cleaves at the C-terminal region of TAFI and reduces its activation to TAFIa Salmonella enterica subsp. enterica serovar Typhimurium TAFIa + ?
-
 ?
3.4.23.49 TAFI + H2O cleaves at the C-terminal region of TAFI Salmonella enterica subsp. enterica serovar Typhimurium TAFIa + ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme PgtE cleaves the tissue factor pathway inhibitor, TFPI Salmonella enterica subsp. enterica serovar Typhimurium ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme PgtE cleaves the tissue factor pathway inhibitor, TFPI Salmonella enterica subsp. enterica serovar Typhimurium SGSC1412 ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O
-
 Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 ?
-
 ?
3.4.23.49 tissue factor pathway inhibitor + H2O TFPI is a major anticoagulant and forms stable TFPI-FXa complexes that block blood clotting. Enzyme PgtE cleaves the tissue factor pathway inhibitor, TFPI Salmonella enterica subsp. enterica serovar Typhimurium ATCC 700720 ?
-
 ?

Synonyms

EC Number Synonyms Comment Organism
3.4.23.48 Pla
-
 Yersinia pestis
3.4.23.49 PgtE
-
 Salmonella enterica subsp. enterica serovar Typhimurium

Expression

EC Number Organism Comment Expression
3.4.23.48 Yersinia pestis expression of Pla is partially repressed in glucose-containing medium down
3.4.23.48 Yersinia pestis transcription of pla is controlled by the cAMP receptor protein Crp additional information
3.4.23.49 Salmonella enterica subsp. enterica serovar Typhimurium PgtE of Salmonella enterica is not expressed under normal laboratory conditions, but the transcription of pgtE is high in mouse macrophages where the degradation of alpha2AP by Salmonella enterica cells also is high. Expression of PgtE is regulated by the SlyA regulator additional information

General Information

EC Number General Information Comment Organism
3.4.23.48 metabolism plasminogen is an abundant circulating zymogen of the serine protease plasmin, which is the key enzyme in fibrinolysis. The physiological plasminogen activation by uPA (EC 3.4.21.73) or tPA (EC 3.4.21.68) is a single cut at the peptide bond R560-V561, which yields the two-chain active plasmin enzyme. Pla rapidly cleaves the same peptide as do the human physiological activators, and the formed plasmin remains enzymatically active as Pla does not degrade the B chain of plasmin that contains the protease catalytic domain Yersinia pestis
3.4.23.48 physiological function Pla of the enteropathogen Yersinia pestis is a surface-exposed, transmembrane beta-barrel proteases of the omptin family that exhibit a complex array of interactions with the hemostatic systems in vitro, the protease is an established virulence factor. Pla favors fibrinolysis by direct activation of plasminogen, inactivation of the serpins plasminogen activator inhibitor-1 and alpha2-antiplasmin, inactivation of the thrombin-activable fibrinolysis inhibitor, and activation of single-chain urokinase. Inactivation of alpha2AP enables proteolysis by the Pla-generated plasmin. The enzymatic activity of the protease is strongly influenced by the environment-induced variations in lipopolysaccharide that binds to the beta-barrel. The protease cleaves the tissue factor pathway inhibitor and thus also expresses procoagulant activity. Some of the functions observed for Pla, such as adhesiveness to laminin and invasiveness into human cells as well as efficient plasmin generation are not shown by PgtE (EC 3.4.23.49) or OmpT. Pla is adapted to support efficient plasminogen activation in the bubonic plague and to enhance bacterial survival in the lungs Yersinia pestis
3.4.23.49 metabolism expression of PgtE is regulated by the SlyA regulator, which, on the other hand, is regulated by the PhoP/Q regulatory system which senses and responses to alpha-helical cationic antimicrobial peptides that are substrates for PgtE degradation Salmonella enterica subsp. enterica serovar Typhimurium
3.4.23.49 physiological function PgtE of the enteropathogen Salmonella enterica is a surface-exposed, transmembrane beta-barrel proteases of the omptin family that exhibit a complex array of interactions with the hemostatic systems in vitro, the protease is an established virulence factor. PgtE proteolysis targets control aspects of fibrinolysis, and mimicry of matrix metalloproteinases enhances cell migration that should favor the intracellular spread of the bacterium. The enzymatic activity of the protease is strongly influenced by the environment-induced variations in lipopolysaccharide that binds to the beta-barrel. The protease cleaves the tissue factor pathway inhibitor and thus also expresses procoagulant activity. PgtE effectively suppresses the regulatory proteins PAI-1, alpha2AP, and TAFI and activates scu-PA to active urokinase. PgtE addresses the control systems rather than direct plasminogen activation. Another mechanism by which PgtE can enhance cell motility and bacteria-phagocyte encounters is its ability to degrade gelatine and to activate the matrix metalloproteinase 9 (procollagenase) secreted from macrophages. PgtE also enhances multiplication of Salmonella enterica inside murine macrophages, where degradation of cationic antimicrobial peptides seems an important function of PgtE. PgtE also inactivates the complement regulatory proteins factors B and H and reduces opsonophacytosis of Salmonella enterica Salmonella enterica subsp. enterica serovar Typhimurium