Coagulation Factor VIII (F8) ELISA Kits

Zebrafish Coagulation Factor VIII (F8) interaction partners

1. gene is flanked by factor VII and factor X genes; gene encodes a protein homologous to factor VII, but lacks critical residues for factor VII activity; functions as an inhibitor of blood coagulation in biochemical assays using zebrafish or human plasmas

Mouse (Murine) Coagulation Factor VIII (F8) interaction partners

1. The increased immunogenicity of oxidized FVIII was not reverted by treatment of mice with N-acetyl cysteine, and did not implicate an increased maturation of professional antigen-presenting cells. Data document that oxidation influences the immunogenicity of therapeutic FVIII.

2. Haemophilic animals (F8(-/-) mice) fed a high fat/fructose diet are highly prone to hepatic steatosis and thrombocytopenia.

3. CD32 blockade suppresses the FVIII-specific recall response by two ways: i) increasing apoptosis of FVIII-specific memory B-cells and ii) disturbing FVIII-specific T cell response by modulating presentation of rhFVIII to CD4(+) T cells.

4. Type 2N von Willebrand disease variants were associated with decreased VWF secretion and impaired factor VIII binding/stability.

5. Cytokine release was quantified from FVIII(-/-) splenocytes restimulated with FVIII in the absence or presence of different anti-FcgammaRIIB (CD32) Antibodies (anti-CD32 mAbs) over 6 days.

6. results revealed localized vascular expression of FVIII and von Willebrand factor and identified lymphatic endothelial cell as a major cellular source of FVIII in extrahepatic tissues.

7. the results indicate that residues in the C1 and/or C2 domains of factor VIII are implicated in immunogenic factor VIII uptake, at least in vitro Conversely, in vivo, the binding to endogenous von Willebrand factor masks the reducing effect of mutations in the C domains on factor VIII immunogenicity.

8. Describe a genetically engineered mouse model of hemophilia A with complete deletion of the F8 gene.

9. data demonstrate that infusion of platelets containing FVIII triggers neither primary nor memory anti-FVIII immune response in FVIII(null) mice

10. Both platelet-VWF and plasma-VWF are required for optimal platelet-derived FVIII gene therapy for hemophilia A in the presence of inhibitors.

11. These data support the investigation of FVIII orthologs as treatment modalities in both the congenital and acquired FVIII inhibitor settings.

12. Extrahepatic sources of factor VIII potentially contribute to the coagulation cascade correcting the bleeding phenotype of mice with hemophilia A.

13. Activatable bioengineered FIX molecules with FVIII-independent activity might be a promising tool for improving hemophilia A treatment, especially for patients with inhibitors.

14. This study demonstrated that FVIIIa interacts with Low-density lipoprotein receptor-related protein 1 cluster III.

15. a fragment containing only approximately 20% of the VWF sequence is sufficient to support FVIII stability in vivo

16. Endothelial cells from multiple, but not all, tissues contribute to the plasma FVIII pool in the mouse.

17. Endothelial cells are the predominant, and possibly exclusive, source of plasma FVIII.

18. Micro-computed tomography analysis of distal tibia metaphyses also revealed for the first time a major impact of the FVIII/thrombin/PAR1 axis on the dynamic bone structure, showing reduced bone.

19. 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.

20. Acute elevations in FVIII levels result in a non-linear thrombogenic effect, with non-significant increases in thrombogenic risk. Prolonged elevation of plasma FVIII did not further increase the thrombogenic potential of elevated FVIII levels.

Human Coagulation Factor VIII (F8) interaction partners

1. Our study suggests that deep intronic variant of c.5999-277G>A may be a hot spot mutation for mild hemophilia patients without mutation in exonic DNA.

2. Development of Factor VIII Inhibitor in a Patient with an Uncommon de novo Mutation in the Factor VIII Gene.

3. Cirrhosis-induced plasma hypercoagulability can be partly explained by opposite changes in two factors: protein C level decrease and FVIII level increase.

4. The combination of a high factor VIII and a low protein C increased coronary heart disease risk synergistically.

5. The K408 in the A2 domain of factor VIII provides an interactive-site for FX in the factor Xase complex.

6. The impact of F8 mutations in non-severe hemophilia A patients on the protein structure and hence, diagnostic bioassay accuracy, has been evaluated.

7. The type of F8 mutation is the main predictor of inhibitor development in patients with severe hemophilia A. Findings confirm an association between the synthesis of minute amounts of FVIII and inhibitor protection.

8. the fraction of mosaic cells with an F8 promoter deletion may affect phenotype severity in a family with hemophilia A

9. results provide novel insights on the adsorption and binding mechanism of the FVIII on cell membrane and will be helpful for the design of anticoagulant materials

10. The D' domain of von Willebrand factor requires the presence of the D3 domain for optimal factor VIII binding.

11. We demonstrated a high concordance in an appreciable number of siblings that developed inhibitors to FVIII or not. The presence of Inv22 and Inv1 in our population was associated to a moderate risk of developing inhibitors.

12. Clustered F8 missense mutations cause hemophilia A by combined alteration of splicing and protein biosynthesis and activity

13. Differential impacts of ectopic N-glycosylation on FVIII folding, trafficking and activity, which highlight complex disease-causing mechanisms of FVIII missense mutations.

14. This study describes an original pathological mechanism by which a small intronic deletion in F8 leads to Alu exonization.

15. A common polymorphism decreases LRP1 mRNA stability and is associated with increased plasma factor VIII levels

16. F8 and F9 gene variants result from a founder effect in two large French haemophilia cohorts

17. our results demonstrate that the N-glycosylation sequon in the A2 domain is located in a structural element that is critically required for proper folding and conformation of FVIII.

18. The aim of this study was to determine the F8 mutations in severe HA (sHA) patients and female carriers

19. Human FVIII gene transfer without in vivo selection of manipulated cells can introduce immune tolerance in hemophilia A mice and this immune tolerance is CD4(+) T cell mediated.

20. In Factor VIII, 41 mutations were identified, 19 of which were novel and 80% (44/55) of the pathogenic mutations fell into the categories of missense, nonsense(16.36%), frameshift (14.55%), and splice (5.45%) mutations.

Pig (Porcine) Coagulation Factor VIII (F8) interaction partners

1. It was concluded that VEGF and factor VIII are important growth factors associated with fetal development in pigs and are identified in all uterine segments.

2. Report Factor VIII organisation on nanodiscs with different lipid composition.

3. thrombin stimulates transglutaminase activity in articular cartilage by directly cleaving factor XIII and by receptor-mediated up-regulation of factor XIII synthesis

4. cupredoxin-like A1 subdomains in fVIII contain inter-species differences that are a result of selective pressure on the dissociation rate constant

Cow (Bovine) Coagulation Factor VIII (F8) interaction partners

1. two factor VIII missense mutations are associated with a mild form of haemophilia A in German Fleckvieh cattle

2. Factor VIIIc is responsible for tissue invasion during tumor progression.

3. A missense mutation (p.Leu2153His) of the factor VIII gene causes cattle haemophilia A.