Recombinant Human Factor IX Protein (C-6His)

Name: Recombinant Human Factor IX Protein (C-6His)
Brand: Beta LifeScience
SKU: BL-1610NP
Availability: InStock

BL-1610NP: Greater than 95% as determined by reducing SDS-PAGE. (QC verified)

Collections: High-quality recombinant proteins, Other recombinant proteins

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Product Overview

Description	Recombinant Human Coagulation Factor IX is produced by our Mammalian expression system and the target gene encoding Thr29-Thr461 is expressed with a 6His tag at the C-terminus.
Accession	P00740
Synonym	F9; Coagulation factor IX; Christmas factor;Plasma thromboplastin component; Coagulation factor IXa light chain; Coagulation factor IXa heavy chain
Gene Background	Coagulation factor IX（F9), is a member of the peptidase S1 family. It contains two EGF-like domains, a Gla domain and a peptidase S1 domain. It is primarily expressed in the liver and secreted in plasma. 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 Ca2+ ions, phospholipids, and factor VIIIa. Mutations in position 43 and 46 prevents cleavage of the propeptide, mutation in position 93 probably fails to bind to cell membranes, mutation in position 191 or in position 226 prevent cleavage of the activation peptide. Mutations of human F9 can result in thrombophilia and recessive X-linked hemophilia B (HEMB). An X-linked blood coagulation disorder characterized by a permanent tendency to hemorrhage, due to factor IX deficiency. It is phenotypically similar to hemophilia A, but patients present with fewer symptoms. Many patients are asymptomatic until the hemostatic system is stressed by surgery or trauma.
Molecular Mass	49.8 KDa
Apmol Mass	60-90 KDa, reducing conditions
Formulation	Supplied as a 0.2 μm filtered solution of 20mM Tris-HCl, 150mM NaCl, 10% Glycerol, pH 8.0.
Endotoxin	Less than 0.1 ng/µg (1 EU/µg) as determined by LAL test.
Purity	Greater than 95% as determined by reducing SDS-PAGE. (QC verified)
Biological Activity	Not tested
Reconstitution
Storage	Store at ≤-70°C, stable for 6 months after receipt. Store at ≤-70°C, stable for 3 months under sterile conditions after opening. Please minimize freeze-thaw cycles.
Shipping	The product is shipped on dry ice/polar packs. Upon receipt, store it immediately at the temperature listed below.
Usage	For Research Use Only

Target Details

Target 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.
Subcellular Location	Secreted.
Protein Families	Peptidase S1 family
Database References	HGNC: 3551 OMIM: 300746 KEGG: hsa:2158 STRING: 9606.ENSP00000218099 UniGene: Hs.522798
Associated Diseases	Hemophilia B (HEMB); Thrombophilia, X-linked, due to factor IX defect (THPH8)
Tissue Specificity	Detected in blood plasma (at protein level). Synthesized primarily in the liver and secreted in plasma.

Gene Functions References

available to predict the inhibitory activity on FIXa. On the basis of pharmacophore modeling, molecular docking, and 3D-QSAR modeling screening, six molecules are PMID: 29724133
Report induced pluripotent stem cell model characterizing mutated F9 mRNA in hemophilia B. PMID: 28834196
genetic association studies in cohort of patients in Switzerland: Data suggest that F9 propeptide mutation-associated hypersensitivity to vitamin K antagonist anticoagulants is rare phenomenon; F9 propeptide mutation Ala37Thr confers high sensitivity to warfarin. PMID: 29450643
Higher FIX antigen levels are associated with incident coronary heart disease in blacks but not in whites; the association of FXI levels with ischemic stroke is slightly attenuated after adjusting for stroke risk factors. PMID: 28393470
a computational approach was conducted to select suitable location(s) for introducing new N-glycosylation sites into the human coagulation factor IX. PMID: 27356208
The pathogenic basis for one synonymous mutation (Val107Val) in the F9 gene associated with haemophilia B was determined. PMID: 28007939
caspase-3 inhibitors also suppressed the attenuation of cell adhesion and phosphorylation of p38 MAPK by EGF-F9. Our data indicated that EGF-F9 activated signals for apoptosis and induced de-adhesion in a caspase-3 dependent manner. PMID: 27129300
Specific factor IX mRNA and protein features that favor drug-induced readthrough over recurrent nonsense mutations have been reported. PMID: 28196793
Here we optimize the transient transfection of HEK293T/17 cells for the production of AAV human factor IX in a disposable fixed-bed bioreactor, the iCELLis((R)) Nano (PALL Corporation). PMID: 27229773
Thus, splicing and protein alterations contribute to define at the molecular level the disease-causing effect of a number of exonic mutations in coagulation FIX exon 5. In addition, our results have a significant impact in the development of splicing-switching therapies in particular for mutations that affect both splicing and protein function PMID: 27227676
This study confirms the high heterogeneity of molecular defects leading to hemophilia B in Belgium. Six missense variants and 1 in-frame deletion, previously unreported, were predicted to affect FIX protein function. PMID: 27865967
this study shows that targeted high-throughput sequencing is an effective technique to detect the F9 gene mutations in hemophilia patients PMID: 27292088
Patient 1 had a 149-kb deletion with breakpoints 90-kb upstream and 30-kb downstream from F9. Patients 2 and 3 showed 273-kb and 1.19-Mb deletions respectively. Patient 4 had two deleted regions: a 1663-bp deletion 1.34-Mb upstream from F9 and a 7.2-Mb deletion including F9. PMID: 26686734
Factor IX mutation was found in every family: eight had large deletions, three had small deletions (<10 base pair) and 102 had single base pair substitutions (69 missense, 26 nonsense, four splice site and three promoter). PMID: 26612714
Data suggest that coagulation factor IX (hFIX) minigene containing beta-globin (hBG) introns could represent a particular interest in stem cell-based gene therapy of hemophilias. PMID: 26928674
miR-128 and miR-125 could help to increase the nonsense-mutant F9 levels by repressing nonsense-mediated mRNA decay. PMID: 27133073
In 293T cells, the addition of 0.5 mM Ca(+2) and 1 mM Mg(+2) resulted in higher recombinant human Factor IX concentration. SK-Hep-1 cell line proved to be very effective in rhFIX production, and it can be used as a novel biotechnological platform for the production of recombinant proteins. PMID: 26802680
Mutations were revealed in 56 unrelated patients with hemophilia B in this study by using direct sequencing of factor IX gene functionally important fragments. PMID: 27529981
The Cys109Tyr F9 mutation found in two siblings and their mother, is a missense mutation previously described in two patients with hemophilia B, but first in Korea. PMID: 25402191
Differentiation studies demonstrated osteogenic (but not chondrogenic or adipogenic) differentiation capability and efficient FIX secretion of the enclosed MSCs in the fibronectin-alginate suspension culture. PMID: 24564349
Selective disruption of exosite-mediated regulation of factor IX by heparin and antithrombin can be achieved with preserved or enhanced thrombin generation capacity. PMID: 25851619
study revealed six unique and unreported changes in the F9 gene among haemophilia B patients from Macedonia and Bulgaria PMID: 25582609
We conclude that the nature of the F9 gene mutation may be an important risk factor for the development of inhibitors. PMID: 25470321
Activatable bioengineered FIX molecules with FVIII-independent activity might be a promising tool for improving hemophilia A treatment, especially for patients with inhibitors. PMID: 25224783
Data suggest that Gly317 plays role in normal catalytic function for FIX/FIXa in the clotting cascade; mutations in Gly317 (G317R, G317E) result in variable severity of bleeding in hemophilia B patients. PMID: 26023895
repetitive elements and non-B DNA forming motifs contribute to deletion mutations in severe haemophilia B PMID: 24816826
Various factor IX mutations have been identified in Chinese hemophilia B patients. PMID: 24261420
11 FIX gene mutations (8 point mutations, 2 small deletions/insertions, and 1 large deletion), including two novel mutations (exon6 c.687-695, del 9 mer and c.460-461, ins T) were found. PMID: 24656159
Report oral FIX gene transfer strategy for hemophilia B. PMID: 24679056
This review discuss structural features of factor XIa that are required for factor IX activation, and the importance of the protease's dimeric structure. [review] PMID: 24759143
Circulating contact-pathway-activating microparticles together with factors IXa and XIa induce spontaneous clotting in plasma of hematology and cardiologic patients. PMID: 24498168
Thrombin-mediated, TAFI-dependent down-regulation of fibrinolysis provides new clues for explaining the heightened thrombotic risk in subjects carrying the FIX-Padua mutation. PMID: 24136406
87 unique mutations (9 novel) were found in 225 American hemophilia B patients. c.316G>A, c.1025C>T, and c.1328T>A accounted 37.1%. Only those with large deletions and nonsense mutations had inhibitors. PMID: 24375831
The allosteric mechanism of activation of antithrombin as an inhibitor of factor IXa and factor Xa: heparin-independent full activation through mutations adjacent to helix D. PMID: 24068708
The results suggest the Omega-loop of FIX binds to an area on FXIa composed of residues from the N-terminus and C-terminus of the A3 domain. These residues are buried in zymogen FXI, and must be exposed upon conversion to FXIa to permit FIX binding. PMID: 23617568
Report interactive database providing insights into mechanisms of hemophilia B. PMID: 23617593
Data indicate that five nanofilters can be used interchangeably to yield a high purity Coagulation Factor IX product. PMID: 23410583
Elevated factor IX activity is associated with an increased odds ratio for both arterial and venous thrombotic events. PMID: 24124147
Letter: report factor IX activity/antigen ratio in relation to risk of first unprovoked venous thromboembolism. PMID: 23446552
Mutations at the -5/-6 site (nucleotides -5 and -6 relative to the transcription start site, designated 1) of the F9 promotor account for the majority of hemophilia B Leyden cases and disrupt the binding of ONECUT transcription factors. PMID: 23472758
Results demonstrate the role of plasticity in regulating FIXa function with respect to discrimination of extended substrate sequences. PMID: 22212890
structural features within residues of the 39-loop contribute to the resistance of FIXa to inhibition by plasma inhibitors ZPI and TFPI. PMID: 23530052
Report causative F9 mutations in Argentine families with hemophilia B and determine mutation-associated FIX inhibitor risks. PMID: 23093250
The effect of surface contact activation and temperature on plasma coagulation with an RNA aptamer directed against factor IXa. PMID: 23054460
investigated the contribution of the NH2-terminal EGF-domain (EGF1) to the recognition specificity of intrinsic tenase by constructing an EGF1 deletion mutant and characterising the properties of the mutant in kinetic, direct binding and FRET assays PMID: 23014580
The results suggest that information at the mRNA level as well as conservation of amino acids of coagulation factor IX correlate well with disease severity. PMID: 22639855
Results indicate that fXIa activates fIX by an exosite- and Ca(2+)-mediated release-rebind mechanism. PMID: 22961984
Western blotting of plasma from FIX deficient (Hemophilia B) patients revealed traces of full-length FIX for the p.R294* and p.R298* mutations, but not for the p.L103* mutation that triggered major FIX mRNA decay. PMID: 22618954
factor IX mutations were identified in either the exon or intronic regions in haemophilia B patients in Malaysia; one novel mutation, 6660_6664delTTCTT was identified in siblings with moderate form of haemophilia B PMID: 22870602
The F9 mutations were heterogenous and the missense mutations were the most prevalent gene defects in Chinese haemophilia B patients. PMID: 22544209

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