EC Number   |
General Information |
Reference |
|---|
   3.4.21.35 | malfunction |
cortical collecting ducts s from tissue kallikrein deficient mice reabsorb potassium. Colonic H+, K+-ATPase activity is increased in intercalated cells of cortical collecting ducts from tissue kallikrein deficient mice |
718318 |
| 3.4.21.35 | malfunction |
enzyme inhibition accelerates the initial virus-induced apoptotic depletion of alveolar macrophages |
752446 |
| 3.4.21.35 | malfunction |
genetically ablating tissue kallikrein in mice results in dilated decompensated cardiomyopathy |
707619 |
| 3.4.21.35 | malfunction |
human tissue kallikrein 1 (KLK1) silencing reduces proangiogenic cell's migratory, invasive, and proangiogenic activities |
717501 |
| 3.4.21.35 | malfunction |
molecular knockdown of endogenous KLK1 expression attenuates advanced glycation end-products-induced interleukin-8 and intercellular adhesion molecule-1 productions in vitro |
732782 |
| 3.4.21.35 | malfunction |
partial or total deficiency in tissue kallikrein induces resistance to the infarct size reducing effect of cyclosporin A in cardiac ischemia in mice |
731281 |
| 3.4.21.35 | malfunction |
tissue kallkrein deficient mice exhibit net transepithelial potassium absorption in cortical collecting ducts because of abnormal activation of the colonic H+,K+-ATPase in intercalated cells and reduced potassium secretion by principal cells secondary to decreased epithelial sodium channel activity |
717526 |
| 3.4.21.35 | physiological function |
beneficial effects of kallidinogenase on increased retinal vascular permeability and vascular endothelial growth factor in diabetic rats. Improvement in abnormal NO metabolism by kallidinogenase suggesting that the kallikrein-kinin system disturbance is corrected |
708396 |
| 3.4.21.35 | physiological function |
elicits a hypotensive action. It is effective in the treatment of patients with acute brain infarction when injected within 48 h after stroke onset. Overexpression of human tissue kallikrein in transgenic rats causes a decrease of isoproterenol-induced cardiac hypertrophy and fibrosis. Human tissue kallikrein gene transfer rescues ischemic tissues in normal mice, and in hypertensive or diabetic animals. Transgenic rats expressing human tissue kallikrein have reduced interstitial fibrosis. Intracerebro-ventribular injection of adenovirus carrying the human tissue kallikrein gene immediately after reperfusion provides neuroprotection against cerebral ischemia injury in a rat model with middle cerebral artery occlusion and in cultured cells by enhancing glial cell migration and inhibiting apoptosis through suppression of oxidative stress and activation of Akt-Bcl-2 signaling pathway |
707619 |
| 3.4.21.35 | physiological function |
exogenous tissue kallikrein attenuates the cerebral ischemia/reperfusion induced rat hippocampal CA1 neurons injury through activating the beta-arrestin-2 assembled B2R-Raf-MEK1/2 signaling module |
732367 |
