Kininogen Deficient – Depleted Plasma
Kininogen Deficient – Depleted Plasma is manufactured from normal citrated human plasma that has been depleted of KN – Kininogen by selective affinity immuno-adsorption using antibodies directed towards KN.
Only the highest quality citrated plasma is used as starting material and in many cases the parent plasma is available as control material. Plasma products are typically buffered with the addition of HEPES to 20mM final concentration and are available in 1ml vials to litre quantities. Our Kininogen deficient – depleted plasma can be used for further manufacturing or research use only applications.
Product Code: KN-DP
Presentation: Frozen Kininogen Deficient – Depleted Plasma
Preparation/Handling: Thaw 1 ml vials in 37oC waterbath for 5 minutes; for bulk volumes, thawing time will be dependent on bottle size.
Storage and Stability: Plasma is shipped frozen and should be stored below -60oC. Product is stable until date stated on vial label when stored at -60oC. Once thawed, plasma is stable for 4 hours at 2-8oC in original vial.
Certificate of Analysis: available upon request
Description of Kininogen
Kininogens are multi-function proteins that are involved in the processes of coagulation, anticoagulation, fibrinolysis, inflammation and cell adhesion. Kininogens are produced in the liver but have also been found in platelets, granulocytes, renal tubular cells and skin. Two forms of kininogen are identified in plasma, both of which are the result of differential splicing of a single gene. High molecular weight kininogen (HK), previously known as Fitzgerald Factor, is a single chain glycoprotein of 120 kDa with a plasma concentration of 80 μg/mL (660 nM). Low molecular weight kininogen (LK), also known as α-cysteine protease inhibitor, is a single chain glycoprotein of 68 kDa with a plasma concentration of 160 μg/mL (2.35 μM). HK and LK share a common heavy chain and bradykinin domain, but have unique light chains. It is the light chain of HK that is responsible for the coagulant cofactor activity by binding to anionic surfaces and for the ability to bind the zymogens prekallikrein (PK) and factor XI (FXI). HK is cleaved by kallikrein in several sequential steps that result in the release of a potent vasodilator bradykinin and the conversion to a two-chain form of HK with increased cofactor activity. In plasma, most of the PK and FXI circulate in complex with HK. Activation of PK by FXIIa generates kallikrein, which initiates reciprocal activation of PK and FXI. The presence of HK also serves to protect kallikrein and activated FXI from protease inhibitors such as C1-Inhibitor, but regulation of the system may be accomplished through proteolytic inactivation of the HK cofactor activity by these enzymes.1-2
References and Reviews
- Coleman RW, Schmaier AH; Contact System: A Vascular Biology Modulator With Anticoagulant, Profibrinolytic, Antiadhesive and Proinflammatory Attributes. Blood 90, pp 3819-3843, 1997.
- DeLa Cadena R, Watchtfogel YT, Colman RW, in Hemostasis and Thrombosis, 3rd Edition, eds. RW Colman, J Hirsh, VJ Marder and EW Salzman, pp. 219-240, J.B. Lippincott Co., Philadelphia, 1994.