Inhibitors | Comment | Organism | Structure |
---|---|---|---|
alpha1-protease inhibitor | membrane-bound Pr3 is inhibited almost as rapidly as the soluble Pr3, but inhibition is not complete after 1 h. No interaction between constitutive membrane-bound Pr3 and the inhibitor | Homo sapiens | |
elafin | membrane-bound Pr3 is inhibited almost as rapidly as the soluble Pr3, but inhibition is not complete after 1 h. No interaction between constitutive membrane-bound Pr3 and the inhibitor | Homo sapiens | |
MeO-Suc-AAPA-chloromethyl ketone | irreversible inhibitor, inhibits about 90% of the activity after 2 h. Membrane-bound Pr3 remains bound to the membrane when inhibited by the chloromethyl ketone inhibitor | Homo sapiens |
Localization | Comment | Organism | GeneOntology No. | Textmining |
---|
Organism | UniProt | Comment | Textmining |
---|---|---|---|
Homo sapiens | - |
- |
- |
Purification (Comment) | Organism |
---|---|
- |
Homo sapiens |
Source Tissue | Comment | Organism | Textmining |
---|---|---|---|
polymorphonuclear neutrophil | - |
Homo sapiens | - |
Substrates | Comment Substrates | Organism | Products | Comment (Products) | Rev. | Reac. |
---|---|---|---|---|---|---|
Abz-Val-Ala-Asp-Nvl-Ala-Asp-Arg-Gln-N-(2,4-dinitrophenyl)ethylenediamine + H2O | - |
Homo sapiens | ? | - |
? |
Synonyms | Comment | Organism |
---|---|---|
PR3 | - |
Homo sapiens |
proteinase 3 | - |
Homo sapiens |
Organism | Comment | Expression |
---|---|---|
Homo sapiens | activation with the calcium ionophore A23187 to optimize membrane-bound Pr3 exposure at the cell surface, whereby Pr3 activity increases by 5-20fold. Resting neutrophils have a genetically determined distribution of the protease that results in a bimodal membrane-bound Pr3 expression | up |
General Information | Comment | Organism |
---|---|---|
physiological function | significant Pr3 activity at the surface of activated neutrophils but not at the surface of quiescent neutrophils whatever the constitutive expression. Permanent presence of inactive Pr3 at the surface of quiescent neutrophils, which may explain why Pr3 is a major target of anti-neutrophil cytoplasmic antibodies, whose binding activates neutrophils and triggers inflammation, as in Wegener granulomatosis | Homo sapiens |