Factor IXa Activity Assay Kit (Fluorometric) (ab204727)
Key features and details
- Assay type: Enzyme activity
- Detection method: Fluorescent
- Platform: Microplate reader
- Sample type: Plasma, Purified protein, Serum
Overview
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Product name
Factor IXa Activity Assay Kit (Fluorometric)
See all Factor IX/PTC kits -
Detection method
Fluorescent -
Sample type
Serum, Plasma, Purified protein -
Assay type
Enzyme activity -
Product overview
Factor IXa Activity Assay Kit (Fluorometric) (ab204727) is based on the ability of FIXa to generate FXa. The generated FXa proteolytically cleaves a synthetic substrate and releases a fluorophore, AMC, which can be easily quantified by fluorescence microplate reader. The assay is simple, rapid and can detect activity as low as 10 pg of FIXa in a variety of samples.
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Notes
The coagulation Factor IX (or Christmas factor, EC 3.4.21.22) is a vitamin K-dependent serine protease. Factor IX is produced as an inactive precursor and is activated via cleavage by either factor XIa (contact pathway) or factor VIIa (tissue factor pathway). In the presence of calcium ions and negatively charged membrane phospholipids, activated factor IX (FIXa) then binds to the activated Factor VIII (FVIIIa) and proteolytically activates factor X (FX) to factor Xa (FXa).
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Platform
Microplate reader
Properties
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Storage instructions
Store at -20°C. Please refer to protocols. -
Components 100 tests Enzyme Mix I 1 vial Enzyme Mix II 1 vial FIXa Assay Buffer 1 x 15ml FIXa Enzyme Standard 1 x 10ng FXa Substrate-AMC 1 x 200µl Phospholipids 1 x 600µl -
Research areas
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Function
Factor IX is a vitamin K-dependent plasma protein that participates in the intrinsic pathway of blood coagulation by converting factor X to its active form in the presence of Ca(2+) ions, phospholipids, and factor VIIIa. -
Tissue specificity
Synthesized primarily in the liver and secreted in plasma. -
Involvement in disease
Defects in F9 are the cause of recessive X-linked hemophilia B (HEMB) [MIM:306900]; also known as Christmas disease.
Note=Mutations in position 43 (Oxford-3, San Dimas) and 46 (Cambridge) prevents cleavage of the propeptide, mutation in position 93 (Alabama) probably fails to bind to cell membranes, mutation in position 191 (Chapel-Hill) or in position 226 (Nagoya OR Hilo) prevent cleavage of the activation peptide.
Defects in F9 are the cause of thrombophilia due to factor IX defect (THR-FIX) [MIM:300807]. A hemostatic disorder characterized by a tendency to thrombosis. -
Sequence similarities
Belongs to the peptidase S1 family.
Contains 2 EGF-like domains.
Contains 1 Gla (gamma-carboxy-glutamate) domain.
Contains 1 peptidase S1 domain. -
Domain
Calcium binds to the gamma-carboxyglutamic acid (Gla) residues and, with stronger affinity, to another site, beyond the Gla domain. -
Post-translational
modificationsActivated by factor XIa, which excises the activation peptide.
The iron and 2-oxoglutarate dependent 3-hydroxylation of aspartate and asparagine is (R) stereospecific within EGF domains. -
Cellular localization
Secreted. - Information by UniProt
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Alternative names
- Christmas Disease
- Christmas factor
- Coagulant factor IX
see all