Human Factor XII (FXII) Matched Antibody Pair (ABPR-L015)

Regulatory status: For research use only, not for use in diagnostic procedures.

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Size
Sufficient reagent for 5 x 96 well plates
Sample
Plasma
Species Reactivity
Human
Intended Use
This antibody pair set comes with matched antibody pair to detect and quantify protein level of Human Factor XII
Contents of Kit
1. Capture Antibody (yellow): 0.5 ml of polyclonal affinity purified anti-FXII antibody for coating plates.
2. Detecting Antibody (red): 0.5 ml of peroxidase conjugated polyclonal anti-FXII antibody for detection of captured FXII.
Note: Reagents are sufficient for at least 5×96 well plates using recommended protocols. Antibodies are supplied in a 50% (v/v) glycerol solution for storage at –10 to -20°C. Keep vials tightly capped. Do not store in frost-free freezers
Storage
-10 to -20°C
General Description
Factor XII (F.XII, Hageman factor) is a 76 kDa, single chain glycoprotein produced in the liver. In plasma, F.XII circulates as a protease zymogen at a concentration of approximately 30 µg/ml (400 nM). Upon vascular injury F.XII 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 α F.XIIa, 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 F.XIIa include the zymogens prekallikrein (PK) and factor XI (F.XI) as well as the procofactor high-molecular weight kininogen (HK). The activation of these substrates results in positive feedback activation of F.XII. Further cleavage of αF.XIIa by kallikrein produces the 28 kDa fragment β F.XIIa (Hageman factor fragment). βF.XIIa 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 α2 Antiplasmin, α2 macroglobulin and antithrombin, even in the presence of therapeutic levels of heparin.

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