Disease relevance of LOC292861

• Reversal of renal fibrosis, inflammation, and glomerular hypertrophy by kallikrein gene delivery [1].
• Moreover, kallikrein reversed salt-induced glomerular hypertrophy and inhibited the increase in levels of the cell cycle-inhibitory proteins p21 and p27 [1].
• Two weeks after adenovirus injection, salt-induced glomerular sclerosis, tubular protein cast formation, and monocyte/ macrophage accumulation in the kidney were notably reversed by kallikrein [1].
• The kallikrein/kinin system is beneficial in ischemia/reperfusion injury in heart, controversial in brain, but detrimental in lung, liver, and intestine [2].
• Taurine amplifies renal kallikrein and prevents salt-induced hypertension in Dahl rats [3].

High impact information on LOC292861

• Kallikrein-stimulated renin release was completely abolished by trasylol, whereas bradykinin did not increase renin production, indicating that kallikrein's effect is not mediated via kinin generation [4].
• The data suggest that uterine contraction produced by a homologous kallikrein does not involve kinin formation but results from an action of this serine proteinase upon other accessible systems coupled to the contractile response [5].
• Kallikrein-induced uterine contraction independent of kinin formation [5].
• Rat urinary kallikrein or bradykinin produced dose-dependent contractions of rat uterus but kallikrein was 5-fold more potent than bradykinin [5].
• Kallikrein caused an immediate series of rhythmic contractions which could be increased gradually with subsequent addition of kininogen substrate [5].

Chemical compound and disease context of LOC292861

• This effect is specific because the opiate antagonist does not modify the hypotension elicited by rat urinary kallikrein, bradykinin or nitroglycerin [6].
• The present investigation evaluated the effects of aprotinin, an inhibitor of kallikrein, on blood pressure responses, heart rate, and duration of hypotension induced by acute administration of captopril and enalapril (angiotensin-converting enzyme inhibitors) in anaesthetized spontaneously hypertensive rats [7].
• Deoxycorticosterone (5 mg) and aldosterone (0.25 mg), given to rats for 14 days, increased the urinary excretion of kallikrein and of prostaglandin E-like substance and produced polyuria, but affected neither sodium excretion nor blood pressure [8].
• The control by estradiol of pituitary tumor and cell growth is not correlated with that of kallikrein gene expression [9].
• Kallikrein-like activity in parotid saliva of rats with various forms of arterial hypertension (genuine, renovascular and DOCA salt hypertension) was studied [10].

Biological context of LOC292861

• Such involvement would suggest that kallikrein is not only potentially involved in an important function of brain development, but also available for studies on regenerative medicine for neurons [11].
• Reactive oxygen species (ROS), malondialdehyde, and reduced/oxidized glutathione measurement revealed that the oxidative stress was augmented by kallikrein administration in both ischemic and reperfusion phases [2].
• This 37,000 dalton kallikrein precursor was hybrid-arrested by a kallikrein cDNA encoding tissue kallikrein which was isolated from a rat submandibular gland cDNA library [12].
• They were found to be the protein products of the rKlk2 (tonin) and the rKlk9 genes by amino acid sequence analysis (nomenclature of the genes and proteins of the kallikrein family is according to the proposal of the discussion panel from the participants of the KININ '91 meeting held Sept. 8-14, 1991, in Munich, Germany) [13].
• Esterase A2 fraction could not induce direct contraction of the rat uterus, and A2 did not cause a transient decrease in rat blood pressure when injected iv, both of which are criteria for kallikrein activity [14].

Anatomical context of LOC292861

• Growth-stimulating Effect of Kallikrein on Rat Neural Stem Cells [11].
• We examined the role of the kallikrein/kinin system in acute ischemia/reperfusion renal injury induced by 40 min occlusion of the renal artery followed by reperfusion [2].
• 1. rK10, a weak T-kininogenase isolated from the rat submandibular gland, is a protein belonging to the rat kallikrein family [15].
• It was proposed that kallikrein may also be located on the basal membrane of tubular epithelial cells, where aldosterone can enhance its activity [16].
• Kallikrein was identified in the adrenal glands of the rat [17].

Associations of LOC292861 with chemical compounds

• Since bradykinin B(2)-receptor antagonist, Hoe140, did not suppress the growth-stimulating effect, kallikrein-mediated kinin release does not appear to be involved in this effect [11].
• Kallikrein gene delivery also dramatically reduced collagens I, III, and IV and reticulin deposition, accompanied by a decline in myofibroblast accumulation and transforming growth factor-beta(1) expression [1].
• In addition, kallikrein protected against salt-induced renal injury by diminishing urinary protein and blood urea nitrogen levels [1].
• These protective actions of kallikrein were abolished by icatibant, indicating a B2 receptor-mediated event [1].
• The purified cardiac enzyme has both N-tosyl-L-arginine methyl ester esterolytic and kinin-releasing activities, and displays parallelism with standard curves in a kallikrein radioimmunoassay, indicating it to have immunological identity with tissue kallikrein [18].

Other interactions of LOC292861

• The prostate gland contained only rK9 where it was the major kallikrein-like component [13].
• Direct action of rat urinary kallikrein on rat kidney to release renin [4].
• Kallikrein excretion remained unchanged after arginine vasopressin infusion [19].
• Respective roles of kallikrein and endopeptidase 24.11 in the metabolic pathway of atrial natriuretic peptide in the rat [20].
• A crude preparation of Kallikrein inactivator, which inhibits the gonadotropin-releasing hormone (GnRH)-degrading enzyme(s) from rat hypothalamus and anterior pituitary, was fractionated by passage through an ion-exchange column [21].

Analytical, diagnostic and therapeutic context of LOC292861

• Two cardiac kallikrein precursors, (38 and 40 kDa) were identified from the translation in vitro of heart mRNA by immunoprecipitation and electrophoresis of [35S]methionine-labelled cell-free translation products [18].
• The homogenate was centrifuged at 105,000 g for 60 minutes, and a vascular kininogenase was purified from the supernatant by chromatofocusing, affinity chromatography on immobilized antibodies against rat urinary kallikrein, and gel filtration on Sephadex G-100 [22].
• Antiserum to rat urinary kallikrein detected a single band in a Western blot of conditioned medium and also immunoprecipitated the enzyme [23].
• To determine whether messenger RNA (mRNA) for glandular kallikrein is present in adrenal gland RNA, we used the polymerase chain reaction employing oligonucleotide primers and glandular kallikrein 32P complementary DNA (cDNA) as a probe, which should give a cDNA fragment of 370 bp [17].
• The electrophoretic mobility of eluted submandibular 125I-labelled kallikrein or submandibular glandular kallikrein was not altered after affinity chromatography, as judged by conventional polyacrylamide disc-gel electrophoresis or by polyacrylamide-gel electrophoresis in the presence of sodium dodecyl sulphate [24].

References