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Literature summary for 3.4.23.48 extracted from

  • Yun, T.; Morrissey, J.
    Polyphosphate and omptins: Novel bacterial procoagulant agents (2009), J. Cell. Mol. Med., 13, 4146-4153.
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.23.48

Activating Compound

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

Localization Comment Organism GeneOntology No. Textmining
outer membrane
-
 Yersinia pestis 19867
-

Organism

Organism UniProt Comment Textmining
Yersinia pestis
-
-
-

Substrates and Products (Substrate)

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

Synonyms Comment Organism
Pla
-
 Yersinia pestis
plasminogen activator
-
 Yersinia pestis

Turnover Number [1/s]

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

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