HK (KNG1) gene is mapped to human chromosome 3q27.3. It is a glycoprotein.[1]
High-molecular-weight kininogen (HK) is the substrate and cofactor of the plasma kallikrein-kinin system (KKS). It is present at a concentration of 660 nM on the plasma and binds to platelet GPI-V-IX complex.
Biochem/physiol Actions
High molecular weight kininogen, two chain, is a participant in contact phase activation of the intrinsic blood coagulation cascade that forms a substrate on which blood factor XI is held in proximity to factor XII allowing reciprocal activation of the two factors. It is also involved in the activation of prekallikrein. High molecular weight kininogen binds to proteoglycans on the surface of platelets, endothelial cells, and other cell types. Domain 5 of high molecular weight kininogen inhibits platelet aggregation and angiogenesis.
High-molecular-weight kininogen (HK) inhibits binding of thrombin to platelets.[2]
Packaging
Package size based on protein content
Physical form
Lyophilized from 4 mM sodium acetate, pH 5.3, 0.15 M NaCl
Preparation Note
Prepared by kallikrein digestion of human kininogen. Purified to remove kallikrein and kinin.
The contact system is a potent procoagulant and proinflammatory plasma protease cascade that is initiated by binding ("contact")-induced, auto-activation of factor XII zymogen. Formed active serine protease FXIIa then cleaves plasma prekallikrein to kallikrein that in turn liberates the mediator
Cytoglobin (Cygb) is a cellular haemoprotein belonging to the globin family with ambiguous biological functions. Downregulation of Cygb in many cancers is indicative of its tumour-suppressive role. This is the first report showing the cell cycle regulation of Cygb, which
American journal of respiratory cell and molecular biology, 63(5), 665-680 (2020-08-07)
Chronic perivascular inflammation is a prominent feature in the lungs of idiopathic pulmonary arterial hypertension. Although the proportions of conventional dendritic cells (cDCs) and plasmacytoid DCs are increased in idiopathic pulmonary arterial hypertension lungs, it remains unknown whether activated cDCs
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