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F8 encodes coagulation factor VIII, which participates in the intrinsic pathway of blood coagulation\; factor VIII is a cofactor for factor IXa which, in the presence of Ca+2 and phospholipids, converts factor X to the activated form Xa. Additionally we are shipping Factor VIII Antibodies (337) and Factor VIII Proteins (32) and many more products for this protein.
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gene is flanked by factor VII (show TH ELISA Kits) and factor X genes; gene encodes a protein homologous to factor VII (show TH ELISA Kits), but lacks critical residues for factor VII (show TH ELISA Kits) activity; functions as an inhibitor of blood coagulation in biochemical assays using zebrafish or human plasmas
data demonstrate that infusion of platelets containing FVIII triggers neither primary nor memory anti-FVIII immune response in FVIII(null) mice
Both platelet-VWF (show VWF ELISA Kits) and plasma-VWF (show VWF ELISA Kits) are required for optimal platelet-derived FVIII gene therapy for hemophilia A in the presence of inhibitors.
These data support the investigation of FVIII orthologs as treatment modalities in both the congenital and acquired FVIII inhibitor settings.
Activatable bioengineered FIX molecules with FVIII-independent activity might be a promising tool for improving hemophilia A treatment, especially for patients with inhibitors.
This study demonstrated that FVIIIa interacts with Low-density lipoprotein receptor-related protein 1 (show LRP1 ELISA Kits) cluster III.
a fragment containing only approximately 20% of the VWF (show VWF ELISA Kits) sequence is sufficient to support FVIII stability in vivo
Endothelial cells from multiple, but not all, tissues contribute to the plasma FVIII pool in the mouse.
Endothelial cells are the predominant, and possibly exclusive, source of plasma FVIII.
Micro-computed tomography analysis of distal tibia metaphyses also revealed for the first time a major impact of the FVIII/thrombin (show F2 ELISA Kits)/PAR1 (show F2R ELISA Kits) axis on the dynamic bone structure, showing reduced bone.
Findings indicate that improving protein trans-splicing by inter-chain disulfide bonding is a promising approach for increasing the efficacy of dual-vector based FVIII gene transfer.
although fVIII bound avidly to soluble forms of clusters II and IV from LRP1 (show LRP1 ELISA Kits), only soluble cluster IV competed with the binding of fVIII to full-length LRP1 (show LRP1 ELISA Kits), revealing that cluster IV represents the major fVIII binding site in LRP1 (show LRP1 ELISA Kits).
The FVIII B domain variants, p.D963N, p.S806T, p.G873D, p.H998Q and p.Q1225R may be considered as polymorphism or non-pathologic mutations in patients with Haemophilia A.
In this meta-analysis, we have assessed the association between the FXIII-A Val34Leu polymorphism and intracerebral hemorrhage risk. The results of a combined analysis showed no significant association between the FXIII-A Val34Leu polymorphism and ICH (show COL4a2 ELISA Kits) risk in the overall population. The results of this meta-analysis suggest that the FXIII-A Val34Leu polymorphism is not associated with ICH (show COL4a2 ELISA Kits) risk in a Caucasian population.
von Willebrand factor (show VWF ELISA Kits) binds to the surface of dendritic cells and modulates peptide presentation of factor VIII.
Desmopressin acetate increases F8 plasma concentration in patients with combined deficiency of factors V and VIII (show COX8A ELISA Kits).
37 (70%) of the 53 had discordant antigen-activity ratio, majority of those mutations produced FVIII with low FVIII-specific activity. However, 4 (7.5%) of the 53 mutations produced higher specific activity of FVIII. It is possible that these mutations either produce a secretory defect or an increased metabolic turnover to account for the low levels of FVIII with these mutations.
Platelet-targeted FVIII gene therapy has higher therapeutic efficacy compared to factor VIII replacement therapy may be due to accelerated thrombin (show F2 ELISA Kits) generation.
Letter: report deep intronic variants of factor VII (show TH ELISA Kits) gene in hemophilia A.
Coagulation test results showed that the presence of double Glu113Asp, Arg593Cys mutations has a slightly synergistic effect on FVIII activity.
Report a dose-response relationship between high FVIII levels and risk of death in venous thrombosis patients and in individuals from the general population.
thrombin (show F2 ELISA Kits) stimulates transglutaminase activity in articular cartilage by directly cleaving factor XIII (show UGDH ELISA Kits) and by receptor-mediated up-regulation of factor XIII (show UGDH ELISA Kits) synthesis
cupredoxin-like A1 subdomains in fVIII contain inter-species differences that are a result of selective pressure on the dissociation rate constant
Factor VIIIc (show COX7A2 ELISA Kits) is responsible for tissue invasion during tumor progression.
This gene encodes coagulation factor VIII, which participates in the intrinsic pathway of blood coagulation\; factor VIII is a cofactor for factor IXa which, in the presence of Ca+2 and phospholipids, converts factor X to the activated form Xa. This gene produces two alternatively spliced transcripts. Transcript variant 1 encodes a large glycoprotein, isoform a, which circulates in plasma and associates with von Willebrand factor in a noncovalent complex. This protein undergoes multiple cleavage events. Transcript variant 2 encodes a putative small protein, isoform b, which consists primarily of the phospholipid binding domain of factor VIIIc. This binding domain is essential for coagulant activity. Defects in this gene results in hemophilia A, a common recessive X-linked coagulation disorder.
, procoagulant component
, antihemophilic factor
, coagulation factor VIII
, coagulation factor VIIIc
, factor VIII F8B
, coagulation factor VIII, procoagulant component (hemophilia A)
, factor VIII
, coagulation co-factor