General description

Anti Factor IX antibody, Mouse monoclonal (mouse IgG1 isotype) is derived from the HIX-1 hybridoma produced by the fusion of mouse Sp2/0-Ag14 myeloma cells and splenocytes from BALB/c mice immunized with factor IX purified from human plasma. Factor IX concentration in human plasma ranges between 2.5-5 mg/ml and its half-life is approximately 24 hours. The human factor IX gene is about 40 Kb in size and is localized at the distal end of the X-chromosome.

Specificity

Monoclonal Anti-Factor IX, a divalent cation-independent antibody, recognizes factor IX when used on immunoblots of non-denatured, non-reduced human plasma. It is also useful as paired labeled antibody in sandwich-type immunoassays with Monoclonal anti-Factor IX, clone HIX-5 (Product No. F1020).
This antibody may be used for purification of Factor IX and preparation of Factor IX depleted human plasma.

Immunogen

Factor IX from pooled normal human plasma.

Application

Monoclonal Anti-Factor IX antibody produced in mouse is suitable for ELISA-based assay in detection of FIX Inhibitors and it has been used as a positive control in ELISA. It is also suitable for western blot at a concentration of 2-4μg/mL.

Biochem/physiol Actions

FIX plays a key role in the intrinsic and extrinsic blood coagulation systems. It is synthesized in liver and later upon activation in plasma it gets converted into a serine protease. In second step, FIX undergoes series of complex post-translation modifications such as γ-carboxylation of 12 N-terminal glutamic acid residues, N- and O-linked glycosylation, phosphorylation, β-hydroxylation, sulfation, disulfide bond formation etc. It is secreted into the plasma after completion of post-translation modifications. Hereditary deficiencies or dysfunctions of factor IX cause hemophilia B or "Christmas Disease" (the surname of the first family described). In haemophilia B, FIX showed impaired coagulation and increased tendency to bleed as a reason of mutation in the X chromosome linked FIX gene. Factor IX is synthesized in liver parenchymal cells and requires a post-translational vitamin K-dependent modification in order to become a mature plasma zymogen. When patients lack vitamin-K or take oral anticoagulants that interfere with the metabolism of vitamin-K, a hypocoagulable or antithrombotic state is induced.

Physical form

Solution in 10 mM HEPES, pH 7.4, with 140 mM sodium chloride and 0.05% sodium azide.

Disclaimer

Unless otherwise stated in our catalog or other company documentation accompanying the product(s), our products are intended for research use only and are not to be used for any other purpose, which includes but is not limited to, unauthorized commercial uses, in vitro diagnostic uses, ex vivo or in vivo therapeutic uses or any type of consumption or application to humans or animals.