Disease relevance of Klk6_predicted

• Proteomic analysis reveals alterations in the renal kallikrein pathway during hypoxia-induced hypertension [1].
• These data indicate that EH induces changes in renal protein expression consistent with impairment of vasodilation mediated by the kallikrein-kallistatin pathway and vascular hypertrophy [1].
• Reversal of renal fibrosis, inflammation, and glomerular hypertrophy by kallikrein gene delivery [2].
• The kallikrein/kinin system is beneficial in ischemia/reperfusion injury in heart, controversial in brain, but detrimental in lung, liver, and intestine [3].
• 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 [2].

High impact information on Klk6_predicted

• In contrast, SH-induced changes suggest the kallikrein- and bradykinin-mediated compensatory mechanisms for prevention of hypertension and vascular remodeling [1].
• NH2-terminal amino acid sequences of the light and heavy chains reveal 74-84% identity to rat tissue kallikrein, tonin, and other kallikrein-related enzymes [4].
• Brain kallikrein is inhibited by a series of tissue kallikrein inhibitors with IC50 values similar to those for urinary kallikrein [5].
• 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 [3].
• 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 [3].

Biological context of Klk6_predicted

• These proteinases correspond to the products of the RSKG-7 and the rGK8 genes, as shown by the comparison of their partial amino-acid sequence with that deduced from nucleotide sequences [6].
• 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 [7].
• The enzymatic activity of renal tissue kallikrein (active and total; specifically antagonized by anti-tissue kallikrein antibodies), increased from 4 to 52 weeks in SHR when compared to normotensive Wistar Kyoto (WKY) rats; this increase was associated with a significant increase in blood pressure [8].
• Consequently, a Charon 4A rat genomic library was screened for kallikrein genes by hybridization with rat tissue kallikrein cDNA [9].

Anatomical context of Klk6_predicted

• Growth-stimulating Effect of Kallikrein on Rat Neural Stem Cells [7].
• In conclusion, vascular kinin-mediated symptoms observed during oedematous pancreatitis in the rat are caused by the action of tissue kallikrein in the pancreas whereas an involvement of plasma kallikrein seems to be unlikely [10].
• This suggests that a tissue kallikrein and also a trypsin-like enzyme or perhaps plasma kallikrein are present in rat uterus [11].
• In Western blot analyses, a specific monoclonal antibody to tissue kallikrein (V4D11) identifies GH3-secreted kallikrein as a approximately 39,000 Da protein, slightly larger than approximately 38,000 Da kallikreins of submandibular gland, mouse anterior pituitary cells (AtT 20) or rodent neuroblastoma X glioma hybrid cells (NG108) [12].
• Nitrite and kallikrein levels in dental pulp tissue were higher in diabetic rats 30 days after STZ treatment than in controls, while only nitrite were decreased 90 after of STZ treatment [13].

Associations of Klk6_predicted 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 [7].
• 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 [2].
• In addition, kallikrein protected against salt-induced renal injury by diminishing urinary protein and blood urea nitrogen levels [2].
• These protective actions of kallikrein were abolished by icatibant, indicating a B2 receptor-mediated event [2].
• Renal kallikrein is secreted by the distal connecting tubular cells and all kallikrein-kinin system components are distributed along the collecting ducts in the distal nephron [14].

Analytical, diagnostic and therapeutic context of Klk6_predicted

• Expression in Escherichia coli was detected by direct radioimmunoassay, and recombinant kallikrein of 36 kDa was identified by Western-blot analysis using both polyclonal and monoclonal antibodies to rat tissue kallikrein, and by autoradiography of 14C-labelled L-amino acid-labelled-protein synthesis in the presence of rifampicin [15].
• A rat tissue kallikrein cDNA probe, 534 bases in length and complementary to the 3' end of kallikrein mRNA was first used in Northern blot analysis to demonstrate the existence of tissue kallikrein mRNA in rat kidney [16].

References