Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.21.4 (
trypsin
)
42,187
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
A study on the clinical effects of urokinase in patients with IgA nephropathy is described. Three different methods of administration, including single, continuous, and mixed administration, were employed in this study. Measurements of plasminogen, plasmin and
alpha 2-plasmin inhibitor
levels in plasma were performed during the course of urokinase administration in patients with IgA nephropathy and chronic proliferative glomerulonephritis. Measurements of alpha 1-anti-
trypsin
and alpha 2-macroglobulin levels were also performed in these patients. Urinalysis was performed both before and after administration of urokinase. It was demonstrated that a single shot of urokinase induced a significant fibrinolytic activity in patients with IgA nephropathy, and that a single shot of urokinase was effective in improving proteinuria and/or hematuria in patients with IgA nephropathy. It is concluded that a single shot of urokinase may be useful for treatment of patients with IgA nephropathy.
...
PMID:Effects of a "single shot" of urokinase on fibrinolytic activities in patients with IgA nephropathy. 653 1
This study has examined the interaction between human leukocyte elastase and
alpha 2-plasmin inhibitor
, or C1 inactivator, inhibitors of proteases of the complement, kinin, coagulation, and fibrinolytic enzyme systems. Leukocyte elastase, in catalytic concentrations, progressively inactivates the plasmin inhibitory activity of both inhibitors. The C1s binding function of C1 inactivator is also destroyed by leukocyte elastase. The nature of the molecular events underlying the inactivation of these protease inhibitors was examined by acrylamide gel electrophoresis in the presence of sodium dodecyl sulfate. Loss of functional activity was accompanied by limited proteolytic cleavage of both inhibitors with the production of several characteristic derivative peptide chains. Leukocyte elastase cleaved
alpha 2-plasmin inhibitor
at two separate sites and generated lower molecular weight fragments similar to those produced by bovine
beta-trypsin
. C1 inactivator was hydrolyzed at three different regions on the molecule whereas
beta-trypsin
cleaved two regions in common with leukocyte elastase. These findings suggest that inactivation of
alpha 2-plasmin inhibitor
and C1 inactivator by leukocyte elastase released in the inflammatory reaction may potentiate pathological proteolysis. The limited digestion of these inhibitory proteins by leukocyte elastase may prove useful in studies of their primary structure.
...
PMID:Proteolytic cleavage and inactivation of alpha 2-plasmin inhibitor and C1 inactivator by human polymorphonuclear leukocyte elastase. 698 Aug 81
Hageman factor (HF, factor XII) that has been exposed to Sephadex-ellagic acid gels is a single-chain species (HFea) with amidolytic properties for the synthetic substrate H-D-phenylalanyl-L-pipecolyl-L-arginine p-nitroanilide. Earlier we reported that amidolysis was suppressed by incubation of HFea with specific antiserum. The present study provides additional evidence that the amidolytic properties of preparations of HFea are ascribable to this substance through an examination of a number of protease inhibitors. HFea's amidolytic properties were inhibited by
alpha 2-plasmin inhibitor
, antithrombin III in the presence of heparin, and Cl esterase inhibitor (Cl-INH). Additionally, it was inhibited by popcorn inhibitor, leupeptin, hexadimethrine bromide, protamine sulfate, dansyl-arginine N-(3-ethyl-1,5-pentanediyl) amide (DAPA), diisopropylphosphofluoridate (DFP), aprotinin, and at excessively high concentrations, soybean and lima bean
trypsin
inhibitors. The spectrum of action of agents that did or did not inhibit HFea supports the view that amidolysis by preparations of HFea is attributable to this enzyme. In general, the enzymatically active carboxy-terminal fragment of HF (HFf) was inhibited by the same agents that inhibited HFea, but aprotinin, protamine sulfate and hexadimethrine bromide were more effective against HFf than HFea, while the reverse was true of lima bean trypsin inhibitor.
...
PMID:Studies on the inhibition of ellagic acid-activated Hageman factor (factor XII) and Hageman factor fragments. 744 15
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