Disease relevance of Ctsg_predicted

• Cathepsin G was purified by single-step cation-exchange chromatography from rat polymorphonuclear leukocytes, obtained from the peritoneal cavity after induction of a mild peritonitis [1].
• This study supports the suggestion that the release of cathepsin G by activated neutrophils, f.i. during inflammation, may contribute to thrombus formation by inducing extensive vascular damage [2].
• Because neutrophil proteinases such as elastase and cathepsin G are considered to play a major role in inflammatory tissue damage, the microcirculatory effect of the serine proteinase inhibitor (serpin) Lex032 after ischemia/reperfusion (I/R)-induced pancreatitis was investigated [3].

High impact information on Ctsg_predicted

• Role of protein-tyrosine phosphatase SHP2 in focal adhesion kinase down-regulation during neutrophil cathepsin G-induced cardiomyocytes anoikis [4].
• Cathepsin G (Cat.G), a neutrophil-derived serine protease, has been shown to induce neonatal rat cardiomyocyte detachment and apoptosis by anoikis through caspase-3 dependent pathway [4].
• The neutral protease cathepsin G belongs to a family of hematopoietic serine proteases stored in the azurophil granules of the neutrophil granulocyte [5].
• Biosynthetic labeling, followed by immunoprecipitation, SDS-polyacrylamide gel electrophoresis, and fluorography, showed that carbohydrate-deficient cathepsin G was synthesized as a 29-kDa proform in both cell lines [5].
• Human skin chymotryptic proteinase. Isolation and relation to cathepsin g and rat mast cell proteinase I [6].

Biological context of Ctsg_predicted

• Purification and N-terminal amino-acid sequence analysis of rat polymorphonuclear leukocyte cathepsin G [1].
• Substrate specificity of two chymotrypsin-like proteases from rat mast cells. Studies with peptide 4-nitroanilides and comparison with cathepsin G [7].
• Therefore, we studied capillary permeability and histological tissue damage after intracerebral injection of neutrophil elastase, cathepsin G, heparatinase and plasmin [8].

Anatomical context of Ctsg_predicted

• Susceptibility of soluble and matrix fibronectins to degradation by tissue proteinases, mast cell chymase and cathepsin G [9].
• Effective concentrations for the combined cathepsin G and elastase in the incubation mixture were similar to the concentrations of these enzymes in PMN-conditioned medium that produced cytotoxicity to hepatocytes [10].
• Neutrophil derived cathepsin G induces potentially thrombogenic changes in human endothelial cells: a scanning electron microscopy study in static and dynamic conditions [2].
• In the same stimulated macrophages there was little activity against type I collagen (associated with MMP-13 [collagenase-3] on the basis of Western blotting), no activity suggestive of stromelysin or matrilysin, and no measurable secretion of the serine proteinases, elastase and cathepsin G [11].
• Rat leukocytes from inflammatory peritoneal exudates respond in vitro to a variety of chemotactic and phagocytic stimuli by releasing both elastase and cathepsin G neutral proteinase enzyme activities [12].

Associations of Ctsg_predicted with chemical compounds

• Leucocyte proteinases, e.g. leucocyte elastase and cathepsin G, are inhibited by heparin [13].
• By contrast, the serine protease inhibitors, aprotinin and 4-(2-aminoethyl)-benzene-sulfonyl fluoride, were less effective in inhibiting cathepsin G and elastase activities as well as cytotoxicity caused by the purified proteases or PMN-conditioned medium [10].
• The six half-cystine residues in the mouse mast cell protease are located in the same positions as in the rat mast cell proteases, cathepsin G, and the lymphocyte proteases, suggesting that they all have identical disulfide bond arrangements [14].
• Previous studies showed a higher percentage of neutrophils from vitamin A deficient rats are hypersegmented and contain lower levels of cathepsin G than the neutrophils from control rats [15].
• Collagenases and the serine proteinases elastase and cathepsin G in steroid-induced Pneumocystis carinii pneumonia [16].

Other interactions of Ctsg_predicted

• The effect of THR, but not that of PAR1-AP, was significantly inhibited by hirulog(TM) (60 microg/mL), a specific and stochiometric THR inhibitor or by cathepsin-G (40 mU/mL), an inhibitor of PAR-1 [17].
• Cytotoxicity of either purified enzyme or of conditioned medium could be prevented by plasma alpha-1-antitrypsin or soybean trypsin-chymotrypsin inhibitor, which were also potent inhibitors of enzymic activity of both cathepsin G and elastase [10].
• Levels of myeloperoxidase, lysozyme, cathepsin G, alkaline phosphatase, gamma-glutamyltranspeptidase and N-acetyl-beta-glucosaminidase showed no sex-based differences [18].

Analytical, diagnostic and therapeutic context of Ctsg_predicted

• The turnover of 125I labelled rat polymorphonuclear leukocyte (PMN) cathepsin G with retained enzymatic activity was followed 180 min after an intravenous injection [19].
• When rat PMN cathepsin G was added to normal rat plasma, we could identify 36% bound to alpha 1-macroglobulin (alpha 1M) and 19% bound to alpha 1-inhibitor 3 (alpha 1I3) as judged from analysis of gel filtration chromatography and electroimmunoassay (EIA) with autoradiography [19].
• The activity of beta-glucuronidase increased in the inflamed paw with time after the induction of adjuvant arthritis while that of cathepsin G was elevated as compared to normal in paws removed, 5 but not 22 days after the induction of adjuvant arthritis [20].

References