Rat FIX ELISA Kit | FIX elisa kit
Rat FIX (Coagulation Factor IX) ELISA Kit
Typical Testing Data/Standard Curve (for reference only)
Principle of the Assay: This ELISA kit uses Sandwich-ELISA as the method. The micro ELISA plate provided in this kit has been pre-coated with an antibody specific to Rat FIX. Standards or samples are added to the appropriate micro ELISA plate wells and bound by the specific antibody. Then a biotinylated detection antibody specific for Rat FIX and Avidin-Horseradish Peroxidase (HRP) conjugate is added to each micro plate well successively and incubated. Free components are washed away. The substrate solution is added to each well. Only those wells that contain Rat FIX, biotinylated detection antibody and Avidin-HRP conjugate will appear blue in color. The enzyme-substrate reaction is terminated by the addition of a sulphuric acid solution and the color turns yellow. The optical density (OD) is measured spectrophotometrically at a wavelength of 450 nm +/- 2 nm. The OD value is proportional to the concentration of Rat FIX. You can calculate the concentration of Rat FIX in the samples by comparing the OD of the samples to the standard curve.
NCBI and Uniprot Product Information
NCBI Description
This gene encodes vitamin K-dependent coagulation factor IX that circulates in the blood as an inactive zymogen. This factor is converted to an active form by factor XIa, which excises the activation peptide and thus generates a heavy chain and a light chain held together by one or more disulfide bonds. The role of this activated factor IX in the blood coagulation cascade is to activate factor X to its active form through interactions with Ca+2 ions, membrane phospholipids, and factor VIII. Alterations of this gene, including point mutations, insertions and deletions, cause factor IX deficiency, which is a recessive X-linked disorder, also called hemophilia B or Christmas disease. [provided by RefSeq, Jul 2008]
Uniprot Description
F9: 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. Defects in F9 are the cause of recessive X-linked hemophilia B (HEMB); also known as Christmas disease. 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 (THPH8). A hemostatic disorder characterized by a tendency to thrombosis. Belongs to the peptidase S1 family.
Protein type: Secreted; Secreted, signal peptide; EC 3.4.21.22; Protease
Chromosomal Location of Human Ortholog: Xq27.1-q27.2
Cellular Component: Golgi lumen; endoplasmic reticulum lumen; plasma membrane; extracellular region
Molecular Function: serine-type endopeptidase activity; calcium ion binding
Biological Process: blood coagulation, extrinsic pathway; cellular protein metabolic process; blood coagulation; proteolysis; post-translational protein modification; peptidyl-glutamic acid carboxylation; blood coagulation, intrinsic pathway
Disease: Hemophilia B; Thrombophilia, X-linked, Due To Factor Ix Defect; Coumarin Resistance
