Cathepsin G

Cathepsin G selectively hydrolyzes specific chymotrypsin-like substrates with characteristic kinetic properties for Bz-Tyr-OEt, but is inactive against trypsin, elastase and several chymotrypsin substrates. It exhibits optimal activity at pH 7.5-8.0 toward azo-casein and Bz-DL-Phe-2-ONap^[1].
Cathepsin G activity is differentially modulated by salts and inhibitors, and is immunologically identical to human leukocyte and neutrophil chymotrypsin-like enzymes. Its activity is promoted by MgCl2, NaCl and KCl, suppressed by CaCl2 and Na2SO4, and completely eliminated by high-concentration NaSCN without persistent functional impairment^[1].
Cathepsin G localizes to the granule fraction (44% of total activity) and undisrupted cell fraction in normal human peripheral blood neutrophils and is released in a dose-dependent manner from stimulated neutrophils, confirming its lysosomal granule localization^[2].
Cathepsin G efficiently generates angiotensin II and hydrolyzes the synthetic substrate BTEE, and shows identical electrophoretic mobility and antigenic identity to the angiotensin II-generating protease^[2].
Cathepsin G (10 μM; 20 min) mediates VITT plasma-induced prothrombotic responses, including platelet-dependent thrombus growth in healthy human whole blood under laminar flow, as well as neutrophil-platelet-based NET formation, tissue factor production and thrombin generation^[3].
Cathepsin G acts as a low-affinity agonist of human FPR with a K_d/EC₅₀ of 85 nM, activating chemotaxis and specific intracellular signaling pathways in human phagocytes and increasing T cell random motility^[4].
Cathepsin G (0-10 μg/mL; 0-30 minutes) potently activates washed human platelets, inducing concentration-dependent degranulation, up-regulation of P-selectin, GPIIb/IIIa complex, and GPIV, and near-complete down-regulation of GPIb^[5].
Cathepsin G modulates chemokine activity through proteolytic processing to produce chemoattractants for neutrophils, monocytes and antigen-presenting cells, and activates protease-activated receptor 4 and protease-activated receptor 2 to exert pro-inflammatory and pro-thrombotic effects in vitro^[6].
Cathepsin G regulates antigen processing and presentation to modulate T cell activation and immune responses, increases endothelial and epithelial cell permeability by disrupting junctional proteins, and activates pro-matrix metalloproteinases to mediate matrix remodeling and angiogenesis^[6].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.