antibody

Mouse Anti Factor IX

MBS140107

0.5 mg

230 USD

monoclonal

mouse

nonconjugated

NYRhFIX

western blot, ELISA, immunohistochemistry, enzyme immunoassay

Antibody

Mouse Anti Factor IX

Factor IX

F9 Antibody; Coagulation Factor-IX, Mouse Antibody; Factor-IX

coagulation factor IX preproprotein; 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

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

FA9_HUMAN

Monoclonal

IgG

NYRhFIX

Mouse

461

protein A

1mg/ml in PBS (after reconstitution).

In lyophilized form, for long periods, store at 4 C in a dry environment. After reconstitution, if not intended for use within a month, aliquot and store at -20 C. Antibody is shipped lyophilized at ambient temperature.

ELISA (EIA), Western Blot (WB), Imunohistochemistry (IHC)

Direct ELISA, Western Blot, imunohistochemistry. For W.B. use 1 ug/ml of antibody. By direct ELISA, 1:10,000 dilution will yield 0.5 O.D using alkaline phosphatase conjugated rabbit anti-mouse Ig.

Reconstitution: Reconstitute with H20 to get a 1 mg/ml concentration. Mix gently, wash the sides of the vial and wait 30-60 seconds before use. Immunogen: Human Factor-IX.

MONOCLONAL/POLYCLONAL ANTIBODIES, MISCELLANEOUS ANTIBODIES; Monoclonal Antibodies

Introduction: Factor IX is a glycoprotein, which is synthesized in the liver. The domain structure of factor IX is similar to that of the other vitamin K dependent coagulation factors. The NH2-terminal region contains 12 g-carboxyglutamic acid (gla) residues, which facilitate the calcium dependent binding of factor IX to negatively charged phospholipid surfaces. Two domains which are homologous to epidermal growth factor (EGF) span the region between the NH2-terminal gla domain and the activation peptide (Ala-146 to Arg-180). Factor IX is activated by either factor XIa or the factor VIIa/tissue factor/phospholipid complex. Cleavage at site A yields the intermediate IXa, which is subsequently converted to the fully active form IXab by cleavage at site B. The NH2-terminal light chain (GLA and EGF domains) remains covalently attached to the COOH-terminal heavy chain by a disulfide bond. The serine protease catalytic triad (Ser-365, His 221, Asp-269) is located in the heavy chain. Factor IXab is the catalytic component of the œintrinsic factor Xase complex (factor VIIIa/IXa/Ca2+/phospholipid) which proteolytically activates factor X to factor Xa.

4503649

NP_000124.1

NM_000133.3

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: EC 3.4.21.22; Protease; Secreted, signal peptide; Secreted. Chromosomal Location of Human Ortholog: Xq27.1-q27.2. Cellular Component: endoplasmic reticulum lumen; Golgi 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

0.5 mg

230 USD

1 mg

350