ELISA/assay

Mouse FIX(Coagulation Factor IX)ELISA Kit

MBS2502581

48-Strip-Wells

410 USD

ELISA Kit

Mouse FIX(Coagulation Factor IX)ELISA Kit

FIX

F9 protein; Coagulation factor IX; coagulation factor IX; Christmas factor; F9 p22; FIX F9; factor 9; factor IX F9; plasma thromboplastic component; plasma thromboplastin component; coagulation factor IX; Christmas factor; Plasma thromboplastin component; PTC

FIX

F9; F9; FIX; P19; PTC; HEMB; THPH8; PTC

FA9_HUMAN

Mouse

461

This assay has high sensitivity and excellent specificity for detection of Mouse FIX. No significant cross-reactivity or interference between Mouse FIX and analogues was observed. Note: Limited by current skills and knowledge, it is impossible for us to complete the cross- reactivity detection between Mouse FIX and all the analogues, therefore, cross reaction may still exist.

Store at 4 degree C.

Samples: Serum, Plasma, Biological Fluids. Assay Type: Sandwich. Detection Range: 0.156--10ng/mL. Sensitivity: 0.094ng/mL

Description: The kit is a sandwich enzyme immunoassay for in vitro quantitative measurement of FIX in Mouse serum, plasma and other biological fluids. 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 Mouse 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 Mouse 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 Mouse 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 Mouse FIX. You can calculate the concentration of Mouse FIX in the samples by comparing the OD of the samples to the standard curve.

80479046

AAI09215.1

P00740

47,618 Da

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, Hypusine Formation And Arylsulfatase Activation Pathway (106231); Gamma-carboxylation Of Protein Precursors Pathway (106233); Gamma-carboxylation, Transport, And Amino-terminal Cleavage Of Proteins Pathway (106232); Hemostasis Pathway (106028)

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]

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; EC 3.4.21.22; Protease; Secreted, signal peptide. Chromosomal Location of Human Ortholog: Xq27.1-q27.2. Cellular Component: Golgi lumen; endoplasmic reticulum lumen; extracellular region; plasma membrane. Molecular Function: serine-type endopeptidase activity; calcium ion binding. Biological Process: blood coagulation, extrinsic pathway; cellular protein metabolic process; blood coagulation; post-translational protein modification; proteolysis; blood coagulation, intrinsic pathway; peptidyl-glutamic acid carboxylation. Disease: Hemophilia B; Thrombophilia, X-linked, Due To Factor Ix Defect; Coumarin Resistance

48-Strip-Wells

410 USD

96-Strip-Wells

490