catalog number :
MBS728510
products type :
ELISA Kit
products full name :
Human Coagulation Factor IX ELISA Kit
products short name :
Coagulation Factor IX
other names :
coagulation factor IX; Coagulation factor IX; coagulation factor IX; F9 p22; FIX F9; factor 9; factor IX F9; Christmas factor; plasma thromboplastic component; plasma thromboplastin component; coagulation factor IX; Christmas factor; Plasma thromboplastin component; PTC
other gene names :
F9; F9; FIX; P19; PTC; HEMB; THPH8; PTC
uniprot entry name :
FA9_HUMAN
storage stability :
Store all reagents at 2-8 degree C.
other info1 :
Assay Type: Competitive or Sandwich. Samples: Serum, plasma, Cell Culture Supernatants, body fluid and tissue homogenate. Sensitivity: 0.1 ng/mL.
products categories :
Cardiovascular
products description :
Intended Uses: This FIX ELISA kit is a 1.5 hour solid-phase ELISA designed for the quantitative determination of Human FIX. This ELISA kit for research use only, not for therapeutic or diagnostic applications!. Principle of the Assay: FIX ELISA kit applies the quantitative sandwich enzyme immunoassay technique. The microtiter plate has been pre-coated with a monoclonal antibody specific for FIX. Standards or samples are then added to the microtiter plate wells and FIX if present, will bind to the antibody pre-coated wells. In order to quantitatively determine the amount of FIX present in the sample, a standardized preparation of horseradish peroxidase (HRP)-conjugated polyclonal antibody, specific for FIX are added to each well to "sandwich" the FIX immobilized on the plate. The microtiter plate undergoes incubation, and then the wells are thoroughly washed to remove all unbound components. Next, substrate solutions are added to each well. The enzyme (HRP) and substrate are allowed to react over a short incubation period. Only those wells that contain FIX and enzyme-conjugated antibody will exhibit a change in color. The enzyme-substrate reaction is terminated by addition of a sulphuric acid solution and the color change is measured spectrophotometrically at a wavelength of 450 nm. A standard curve is plotted relating the intensity of the color (O.D.) to the concentration of standards. The FIX concentration in each sample is interpolated from this standard curve.
ncbi acc num :
CCA61112.1
ncbi mol weight :
47,618 Da
ncbi pathways :
Blood Clotting Cascade Pathway (198840); Complement And Coagulation Cascades Pathway (198880); Complement And Coagulation Cascades Pathway (83073); Complement And Coagulation Cascades Pathway (484); Extrinsic Pathway (106058); Formation Of Fibrin Clot (Clotting Cascade) Pathway (106057); Gamma-carboxylation Of Protein Precursors Pathway (106233); Gamma-carboxylation, Transport, And Amino-terminal Cleavage Of Proteins Pathway (106232); Hemostasis Pathway (106028); Intrinsic Pathway (106059)
ncbi summary :
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 summary :
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: Protease; Secreted; Secreted, signal peptide; EC 3.4.21.22. 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; post-translational protein modification; blood coagulation; proteolysis; blood coagulation, intrinsic pathway; peptidyl-glutamic acid carboxylation. Disease: Hemophilia B; Thrombophilia, X-linked, Due To Factor Ix Defect; Coumarin Resistance
size1 :
48-Strip-Wells-(Competitive)
size2 :
48-Strip-Wells-(Sandwich)
size3 :
96-Strip-Wells-(Competitive)
size4 :
96-Strip-Wells-(Sandwich)