Activating Compound | Comment | Organism | Structure |
---|---|---|---|
bacterial lipopolysaccharide | LPS is required for the enzymatic activity of omptins, and in particular, LPS with short O-antigen side chains (rough LPS) is required for omptin activity toward many exogenous macromolecular substrates. It is thought that an extended O-antigen side chain (smooth LPS) sterically interferes with substrate binding | Yersinia pestis |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|---|---|---|---|
outer membrane | - |
Yersinia pestis | 19867 | - |
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Yersinia pestis | - |
- |
- |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
alpha2-antiplasmin + H2O | Pla inactivates the main physiologic inhibitor of plasmin | Yersinia pestis | ? | - |
? | |
complement C3 + H2O | Pla proteolyzes complement C3 which may amiliorate the host inflammatory response by abolishing its chemoattractant properties | Yersinia pestis | ? | - |
? | |
human Glu-plasminogen + H2O | Pla activates Glu-plasminogen to plasmin, in vitro, TFPI is found to be a much better substrate for Pla than plasminogen | Yersinia pestis | plasmin + ? | - |
? | |
human tissue factor pathway inhibitor + H2O | Pla can proteolytically degrade TFPI, completely abrogating its anticoagulant function. In vitro, TFPI is found to be a much better substrate for Pla than plasminogen | Yersinia pestis | ? | - |
? | |
zymogen factor VII + H2O | Pla proteolytically converts zymogen factor VII to the active form, factor VIIa. Pla activates factor VII about twice as fast as it activates plasminogen | Yersinia pestis | factor VIIa | - |
? |
Synonyms | Comment | Organism |
---|---|---|
Pla | - |
Yersinia pestis |
plasminogen activator | - |
Yersinia pestis |
Turnover Number Minimum [1/s] | Turnover Number Maximum [1/s] | Substrate | Comment | Organism | Structure |
---|---|---|---|---|---|
0.0035 | - |
human Glu-plasminogen | pH not specified in the publication, temperature not specified in the publication | Yersinia pestis |
General Information | Comment | Organism |
---|---|---|
malfunction | eliminating Pla expression in a fully virulent Yersinia pestis strain decreases its LD50 by 6 orders of magnitude in a mouse model of bubonic plague | Yersinia pestis |
malfunction | Pla deficient Yersinia pestis disseminate to regional lymph nodes after subcutaneous inoculation but do not cause the lymphadenopathy observed with wild-type Yersinia pestis infections | Yersinia pestis |
malfunction | survival of mice infected with Pla-deficient Yersinia pestis is greater than cohorts infected with wild-type Yersinia Pestis. Survival advantage is negated, if fibrinogen knockout mice are infected instead, directly implicating the host coagulation system as a target for Pla's role in virulence | Yersinia pestis |
physiological function | 1. Pla expression results in attenuated inflammatory cell recruitment (particularly neutrophils) to infected lesions 2. Pla expression causes a structural derangement of infected lymph tissue characterized by lymphadenitis, necrosis, hemorrhage, thrombosis, and disorganized masses of infiltrating bacteria. 3. Pla expression promotes the systemic dissemination of the infection | Yersinia pestis |
physiological function | Pla works to accelerate the initiation phase of blood clotting by activating the first enzyme in blood clotting (factor VIIa) and inactivating its most important protease inhibitor in plasma (TFPI). This is highly reminiscent of the ability of Pla to activate plasminogen to plasmin and to inactivate its plasma inhibitor, alpha2-antiplasmin | Yersinia pestis |