EC Number |
General Information |
Reference |
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3.4.21.20 | malfunction |
abrogation of CatG activity results in functional inhibition of proinsulin-reactive T cells |
718285 |
3.4.21.20 | malfunction |
both pharmacologic inhibition of cathepsin G and its congenital absence prolonge the time for platelet thrombus to form in ferric chloride-injured mouse mesenteric arterioles. In a vaso-occlusive model of ischemic stroke, inhibition of cathepsin G and its congenital absence improves cerebral blood flow, reduces histologic brain injury, and improves neurobehavioral outcome |
732742 |
3.4.21.20 | malfunction |
inhibition of CatG reduces the presentation of antigens to CD4+ T cells |
709983 |
3.4.21.20 | malfunction |
inhibition of cathepsin G reduces active TGF-beta at the tumor-bone interface |
709904 |
3.4.21.20 | malfunction |
the absence of cathepsin G reduces arterial wall elastin degradation and attenuates early atherosclerosis when mice consume a Western diet for 3 months |
731354 |
3.4.21.20 | physiological function |
acts as a major histocompatibility complex calls II-degrading protease, involved in major histocompatibility complex class II turnover |
708698 |
3.4.21.20 | physiological function |
at a concentration of 60 nM, cathepsin G induces a statistically significant acceleration of thrombin generation in blood plasma. With increasing concentrations of cathepsin G, endogenous thrombin potential and thrombin peak decrease also. A statistically significant decrease in all three thrombogram parameters is found at 240 nM. Cathepsin G is not able to induce thrombin generation in factor V- or factor X-depleted plasma |
718414 |
3.4.21.20 | physiological function |
CatG plays a critical role in proinsulin processing and is important in the activation process of diabetogenic T cells |
718285 |
3.4.21.20 | physiological function |
cathepsin G activity lowers plasma low-density lipoprotein and reduces atherosclerosis. The enzyme promotes early atherogenesis through its elastinolytic activity, but suppresses late progression of atherosclerosis by degrading low-density lipoprotein without affecting high-density lipoprotein or triglycerides |
731354 |
3.4.21.20 | physiological function |
cathepsin G is activating pro-MMP9, involved in enhanced TGF-betra signaling |
709904 |