3.4.21.35: tissue kallikrein
This is an abbreviated version!
For detailed information about tissue kallikrein, go to the full flat file.
Word Map on EC 3.4.21.35
Reaction
Preferential cleavage of Arg-/- bonds in small molecule substrates. Highly selective action to release kallidin (lysyl-bradykinin) from kininogen involves hydrolysis of Met-/- or Leu-/-. The rat enzyme is unusual in liberating bradykinin directly from autologous kininogens by cleavage at two Arg-/- bonds
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Synonyms
bradykininogenase, callicrein, depot-Padutin, dilminal D, EC 3.4.21.8, EC 3.4.4.21, EMSP1, GK1, glandular kallikrein, glandular kallikrein 2, glandular kallikrein 24, glandular kallikrein-2, glumorin, HK1, hK10, hK11, hK13, hK14, hK3, hK5, hK6, hK8, HSCTE, HUK, K1, K2, Kailikang, Kal, kallidinogenase, kallikrein, kallikrein 1, kallikrein 24, kallikrein-related peptidase, kallikrein-related peptidase 10, kallikrein-related peptidase 2, kallikrein-related peptidase 7, kidney/pancreas/salivary gland kallikrein, kininogenase, kininogenin, KLK, KLK-L1 protein, KLK-L2 protein, KLK-L3, KLK-S3, KLK1, KLK10, KLK11, KLK15, KLK2, KLK3, KLK4, KLK5, KLK6, KLK7, KLK9, mK1, mK13, mK22, mK24, mK9, More, neurosin, onokrein P., P1 kallikrein, padreatin, padutin, pancreatic kallikrein, pancreatic/renal kallikrein, PPK, Prk, pro-renin-converting enzyme, prokallikrein, prostase, prostase/KLK-L1/ARM1/PRSS17, prostate specific antigen, protease M, PS kallikrein, PSA, PSA/KLK3, renal kallikrein, renal tissue kallikrein, RSGK-50, RUK, S01.160, S1 kallikrein, S2 kallikrein, S3 kallikrein, salivary kallikrein, SEV, skeletal muscle kallikrein, submandibular enzymatic vasoconstrictor, T-kininogenase, tissue kallidinogenase, tissue kallikrein, tissue kallikrein 1, tissue kallikrein 11, tissue kallikrein 15, tissue kallikrein 4, tissue kallikrein 9, TK, trypsin-like serine protease, UKLK, urinary kallidinogenase, urinary kallikrein, urinary tissue kallikrein, urokallikrein, zyme
ECTree
General Information
General Information on EC 3.4.21.35 - tissue kallikrein
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malfunction
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genetically ablating tissue kallikrein in mice results in dilated decompensated cardiomyopathy
malfunction
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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
malfunction
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human tissue kallikrein 1 (KLK1) silencing reduces proangiogenic cell's migratory, invasive, and proangiogenic activities
malfunction
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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
malfunction
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molecular knockdown of endogenous KLK1 expression attenuates advanced glycation end-products-induced interleukin-8 and intercellular adhesion molecule-1 productions in vitro
malfunction
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partial or total deficiency in tissue kallikrein induces resistance to the infarct size reducing effect of cyclosporin A in cardiac ischemia in mice
malfunction
enzyme inhibition accelerates the initial virus-induced apoptotic depletion of alveolar macrophages
physiological function
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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
physiological function
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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
physiological function
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HUK reduces brain damage in experimental stroke: in a mouse middle cerebral artery occlusion model, HUK significantly improves neurofunction, decreases infarct size, and suppresses edema, as well as inflammatory mediators as compared with the vehicle group. Furthermore, HUK inhibits the NF-kappaB pathway and activates the MAPK/ERK pathway in this neuroprotection
physiological function
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oral administration of tissue kallikrein purified from porcine pancreas results in blood pressure reduction in hypertensive patients
physiological function
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pretreatment of cultured cortical neurons from rats with tissue kallikrein largely prevents glutamate-induced morphological changes and cell death: tissue kallikrein pretreatment alleviates glutamate-induced oxidative stress by inhibiting neuronal nitric oxide synthase activity, thereby reducing the generation of nitric oxide and reactive oxygen species. Extracellular signal-regulated kinase 1/2 cascade (ERK1/2), particularly ERK1, and nuclear factor-kappaB are involved in tissue kallikrein neuroprotection against glutamate-induced neurotoxicity. Tissue kallikrein pretreatment activates ERK1 and nuclear factor-kappaB, leading to enhanced expression of brain-derived neurotrophic factor mRNA and antiapoptotic gene Bcl-2 protein
physiological function
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purified tissue kallikrein promotes DU145 prostate cancer cell migration in a similar manner than rat tissue kallikrein
physiological function
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role of the kallikrein-kinin system in diabetic nephropathy
physiological function
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tissue kallikrein has antioxidant characteristics and is capable of alleviating ischemia-acidosis/reperfusion-induced injury, inhibiting apoptosis and promoting cell survival in vitro: pretreatment of cultured cortical neurons from rats with tissue kallikrein reduces cell death induced by either acidosis or oxygen and glucose deprivation-acidosis/reoxygenation. It exerts the neuroprotective effects by reducing production of reactive oxygen species, stabilizing the mitochondrial membrane potential and inhibiting caspase-3 activation, and thereby attenuating oxidative stress and apoptosis. Activation of the extracellular signal-regulated kinase1/2 signaling cascade but not the PI3K/Akt signaling pathway is required for the survival-promoting effect of tissue kallikrein on neurons exposed to oxygen and glucose deprivation-acidosis/reoxygenation
physiological function
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tissue kallikrein promotes cell migration and proliferation of HaCaT keratinocytes in a concentration- and time-dependent manner. Active TK stimulates keratinocyte migration independent of kinin, kinin B2 receptor and NO formation. Tissue kallikrein-induced keratinocyte migration is dependent on PAR1 activation and EGFR phosphorylation. Local application of tissue kallikrein promotes skin wound healing. Signaling pathways mediated by tissue kallikrein promote keratinocyte migration through activation of the PAR1-PKC-Src-MMP pathway and HB-EGF/AR shedding-dependent EGFR transactivation
physiological function
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tissue kallikrein promotes DU145 prostate cancer cell migration in a concentration-dependent manner, but has no effect on A549 lung cancer cells. Tissue kallikrein stimulates DU145 cell proliferation through activation of the kinin B2 receptor, but not PAR1 and EGFR activation. Tissue kallikrein promotes migration and invasion of DU145 cells through PAR1-PKC-Src-MMP activation and EGFR-ERK transactivation. Tissue kallikrein stimulates ERK activation through EGFR transactivation. Differential signaling pathways mediated by tissue kallikrein in promoting prostate cancer cell migration and invasion via PAR1 activation, and proliferation via kinin B2 receptor stimulation. Stimulates ERK phosphorylation
physiological function
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tissue kallikrein/kinin infusion not only prevents but also reverses kidney injury, inflammation and fibrosis in salt-induced hypertensive rats. Wide time window for kallikrein administration in protection against ischemic brain infarction: delayed kallikrein infusion for 24 h after cerebral ischemia in rats is effective in reducing neurological deficits, infarct size, apoptosis and inflammation. Tissue kallikrein induces contraction of isolated rat uterus in the absence of kinin formation, and elicites cardioprotection by direct kinin B2 receptor activation in kininogen-deficient Brown Norway rats. A subdepressor dose of kallikrein protein or kinin peptide restores impaired cardiac function in rats with postinfarction failure by inhibiting hypertrophy and fibrosis and promoting angiogenesis through increased NO formation and inhibition of oxidative stress and TGF-beta expression. Local application of tissue kallikrein promotes skin wound healing in rats
physiological function
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treatment with recombinant adeno-associated virus-tissue kallikrein decreases cell apoptosis in the target organs of spontaneous hypertensive rats and also inhibits lipopolysaccharide-induced HEK-293 apoptosis. The recombinant adeno-associated virus-tissue kallikrein delivery system increases the levels of apoptosis-inhibiting proteins bcl-2 and bcl-x(L), and decreases the level of Bax and the activity of caspase 3, two promoters of apoptosis. In addition to its role in the inhibition of apoptosis, adeno-associated virus-tissue kallikrein activates the cell survival and proliferation signaling pathways ERK1/2 and PI3K/AKT
physiological function
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tumour-induced, vascular-derived tissue kallikrein that surrounds angiogenic endothelial cells likely aids in stromal remodelling to allow angiogenesis and the release of contributing co-factors, contributes to neo-vasculature invasiveness and produces a tempero-spatial chemotactic message that may be recognised by cell signaling systems
physiological function
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human tissue kallikrein is produced and released by gastrointestinal stromal tumor and participates in tumor invasion. Human tissue kallikrein released by gastrointestinal stromal tumor cells promotes endothelial cell migration and network formation through kinin-dependent mechanisms
physiological function
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human tissue kallikrein promotes activation of the ipsilesional sensorimotor cortex after acute cerebral infarction. Tissue kallikrein improves neural function effectively and quickly after stroke, and promoting cerebral reorganization is an important mechanism for tissue kallikrein in the treatment of acute cerebral infarction
physiological function
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tissue kallikrein acts directly on epithelial sodium channel in order to modulate its activity but is not critical for the regulation of renal sodium homeostasis. Tissue kallikrein is a kaliuretic factor that provides a rapid abd aldosterone-independent protection against hyperkalemia after a dietary potassium load
physiological function
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tissue kallikrein inhibits vascular endothelial growth factor-165-induced tube formation, proliferation, and migration in vitro angiogenesis model via suppression of the vascular endothelial growth factor-165-induced phosphorylation of vascular endothelial growth factor receptor-2. Tissue kallikrein is partly involved in pathogenesis of proliferative diabetic retinopathy
physiological function
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tissue kallikrein is a unique kalliuretic factor that protects against hyperkalemia after a dietary potassium load
physiological function
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tissue kallikrein is essential for invasive capacity of circulating proangiogenic cells
physiological function
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tissue kallikrein prevents neurons from hypoxia/reoxygenation damage by influencing the activity of bradykinin B2 receptor followed by activating the ERK1/2 signal pathway, and thus promoting the survival of cortical neurons subjected to ischemia/reperfusion insults
physiological function
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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
physiological function
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tissue kallikrein induces SH-SY5Y cell proliferation via epidermal growth factor receptor and extracellular signal-regulated kinase1/2 pathway
physiological function
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tissue kallikrein is required for the cardioprotective effect of cyclosporin A in myocardial ischemia in the mouse. The enzyme is required for the mitochondrial action of cyclosporin A and may interact with cyclophilin D
physiological function
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tissue kallikrein promotes vessel growth by increasing the number of peripheral endothelial progenitor cells and enhancing their functional properties through the kinin B2 receptor-Akt signaling pathway. The enzyme reduces hypoxia-induced apoptosis of peripheral endothelial progenitor cells and increases cardiac function after myocardial infarction
physiological function
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tissue kallikrein reduces cell injury induced by oxygen and glucose deprivation/reoxygenation through activating and increasing the protein expression of Homer1b/c protein
physiological function
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tissue kallikrein treatment significantly reduces monocyte chemoattractant protein-1, intercellular adhesion molecule-1, and interleukin-6 levels in retinal pigment epithelium-choroid complexes. Tissue kallikrein exhibits antiangiogenic properties by cleaving vascular endothelial growth factor 164 in a laser-induced choroidal neovascularization model
physiological function
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up-regulation of KLK1 in tubular epithelial cells may mediate pro-inflammatory pathway and protease-activated receptor activation during diabetic nephropathy
physiological function
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the enzyme ameliorates cerebral vasospasm and inhibits apoptosis in the basilar artery in a rabbit model of subarachnoid hemorrhage. The enzyme increases levels of nitric oxide which has a vasodilatory effect, but does not affect levels of endothelin-1, which has a vasoconstrictive effect
physiological function
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the enzyme protects SH-SY5Y neuronal cells against oxygen and glucose deprivation-induced injury through bradykinin B2 receptor-dependent regulation of autophagy induction. The enzyme decreases cell death caused by oxygen and glucose deprivation
physiological function
the enzyme regulates alveolar macrophage apoptosis early in influenza virus infection