Factor XII Deficient – Depleted Plasma
Factor XII Deficient – Depleted Plasma is manufactured from normal citrated human plasma that has been depleted of Factor XII by selective affinity immuno-adsorption using antibodies directed towards FXII.
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 Factor XII Deficient – Depleted Plasma can be used for further manufacturing or research use only applications.
Product Code: FXII-DP
Presentation: Frozen Factor XII Deficient – Depleted Plasma
Preparation/Handling: Thaw 1 ml vials in 37oC water bath 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 Factor XII
Factor XII (FXII, Hageman factor) is a 76 kDa, single chain glycoprotein produced in the liver. In plasma, FXII circulates as a protease zymogen at a concentration of approximately 30 μg/ml (400 nM). Upon vascular injury FXII binds to negatively charged extravascular surfaces such as cartilage and skin, which facilitate activation of the zymogen to the active serine protease. Cleavage of F.XII by kallikrein after residue Arg353 produces the enzyme αFXIIa, consisting of a 28 kDa light chain containing the protease domain, and a 52 kDa heavy chain containing the anionic surface-binding domain. Substrates for surface bound FXIIa include the zymogens prekallikrein (PK) and factor XI (FXI) as well as the procofactor high-molecular weight kininogen (HK). The activation of these substrates results in positive feedback activation of FXII. Further cleavage of αFXIIa by kallikrein produces the 28 kDa fragment βFXIIa (Hageman factor fragment). βFXIIa has reduced procoagulant activity as it lacks the anionic surface-binding domain, but is capable of fluid-phase activation of PK, factor VII and complement C1. The activity of F.XIIa in plasma is regulated predominantly by C1-Inhibitor, with relatively minor contributions by α2antiplasmin, α2macroglobulin and antithrombin, even in the presence of therapeutic levels of heparin1-3.
References and Reviews
- 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.
- Tankersley DL, Alving BM, Finlayson JS; Preparation of βF.XIIa (Hageman Factor Fragment) from Human Plasma. Thrombosis Research 25 pp 307-317, 1982.
- Pixley RA, Schapira M, Coleman RW; The regulation of Human Factor XIIa by Plasma Proteinase Inhibitors. JBC 260, pp 1723-1729, 1985.