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Literature summary for 3.4.23.48 extracted from

  • Smiley, S.T.; Szaba, F.M.; Kummer, L.W.; Duso, D.K.; Lin, J.S.
    Yersinia pestis Pla protein thwarts T cell defense against plague (2019), Infect. Immun., 87, e00126-19 .
    View publication on PubMedView publication on EuropePMC
Search for more literature for 3.4.23.48

Protein Variants

Protein Variants Comment Organism
D206A site-directed mutagenesis, introducing the single point mutation into the active site of Pla suffices to render fully virulent Yersinia pestis susceptible to primed T-cells. The protective capacity of YopE-specific CD8 T cells against CO92 Pla-D206A is abrogated in mice with low levels of tissue factor activity as well as in PAI-1/TAFI double knockout mice. In addition, YopE-specific CD8 T cells poorly protect wild-type mice treated with Coumadin, a pharmacologic anticoagulant that reduces production of fibrin Yersinia pestis

Organism

Organism UniProt Comment Textmining
Yersinia pestis P17811
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-
Yersinia pestis D27 P17811
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-

Synonyms

Synonyms Comment Organism
Pla
-
 Yersinia pestis

General Information

General Information Comment Organism
malfunction introducing the single point mutation D206A into the active site of Pla suffices to render fully virulent Yersinia pestis susceptible to primed T-cells Yersinia pestis
physiological function the plasminogen activator Pla is a protease that promotes fibrin degradation and prevents T cell-mediated defense against fully virulent Yersinia pestis. Pla functions to thwart fibrin-dependent T-cell-mediated defense against plague by promoting fibrinolysis. The presence of primed CD8 T-cells can suffice to protect against a lethal dose (LD) of a virulent Yersinia pestis strain rendered deficient in Pla activity in a fibrin-dependent manner Yersinia pestis