Coagulation Factor X (F10) ELISA Kits

Human Coagulation Factor X (F10) interaction partners

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

2. under flow, TFPI-alpha is capable to antagonize fibrin formation in a manner dependent on and restricted by local TF/factor VIIa and factor Xa activities

3. The identification of 11 novel F10 mutations provides a substantial contribution to the mutations known to cause FXD.

4. F10 mutation spectrum in Pakistan is heterogeneous as seen in other populations

5. Gla-domainless factor Xa binds to TFPI and restores ex vivo coagulation in hemophilia plasma

6. An antidote could promptly neutralize the anticoagulant effects of both FXa inhibitors. Our results suggest that drugs and aptamers with shared targets can be combined to exert more specific and potent effects than either agent alone

7. model predicts that small vesicles promote activation of FX by the extrinsic tenase significantly better than large vesicles

8. miR-24 was overexpressed in major trauma-induced coagulopathy (TIC) patients. The negative correlation of miR-24 with FX suggested the possibility that miR-24 might inhibit the synthesis of FX during TIC.

9. this study demonstrated that thrombin and factor Xa cleavage sites on HEV pORF1 are obligatory for HEV replication.

10. zymogen-like factor Xa variants are conformationally dynamic and ligands such as its cofactor, factor Va, stabilize the molecule rescuing procoagulant activity. At the site of vascular injury, the variants in the presence of factor Va serve as effective prohemostatic agents.

11. Data suggest that, for all coagulation proteins tested (prothrombin, factor X, activated factor VII, activated protein C), tighter binding to lipid bilayers (lower Kd) is observed as the proportion of anionic phospholipid increases. These studies were conducted in high-throughput screening using phospholipid bilayers in nanodiscs with multiplexed silicon photonic sensor (micro-ring resonator) array technology.

12. A coagulation initiating pathway is revealed in which the TF-FVIIa-nascent FXa complex activates FVIII apart from thrombin feedback.

13. Data suggest oxidized lipid vesicles with phosphatidylserine/polyunsaturated fatty acids promote inactivation of ZPI-PZ complex or free ZPI; binding of PZ-complexed or free ZPI to oxidized vesicles mediates inactivation of ZPI (an inhibitor of FXa); blocking heparin- (anticoagulant-)binding site on ZPI interferes with binding to lipid or PZ. (ZPI = protein Z-dependent protease inhibitor; PZ = protein Z; FXa = factor Xa)

14. Factor Va reduced by 100-fold the apparent Kd of myosin for factor Xa (Kd approximately 0.48 nM), primarily by reducing koff, indicating formation of a stable ternary complex of myosin:Xa:Va.

15. PTX2 was identified PTX2 as a novel partner for FX, and both proteins cooperated to prevent their SR-AI-mediated uptake by macrophages.

16. annexin A2 contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa.

17. Individuals suffering from relapsing-remitting and secondary progressive multiple sclerosis had significantly higher prothrombin and factor X levels than healthy donors, whereas levels were unchanged in primary progressive MS and neuromyelitis optica patients.

18. Low concentrations of TF and exogenous FXIa, each too low to elicit a burst in thrombin production alone, act synergistically when in combination to cause substantial thrombin production.

19. A family with factor X deficiency from Argentina displayed a compound heterozygous proband having the combination of a new mutation with an already known one, and homozygous children.

20. analysis of how physiological concentrations of Tissue factor pathway inhibitor inhibit FXa

Mouse (Murine) Coagulation Factor X (F10) interaction partners

1. PTX2 was identified PTX2 as a novel partner for FX, and both proteins cooperated to prevent their SR-AI-mediated uptake by macrophages.

2. annexin A2 contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa.

3. Enhanced FXa and PAR2 exacerbate DN and that both are promising targets for preventing diabetic nephropathy.

4. Macrophages regulate FX plasma levels in an SR-AI-dependent manner.

5. Factor Xa has a role in inhibiting HMGB1-induced septic responses in human umbilical vein endothelial cells and in mice

6. Selective inhibition of FXa improves the left ventricular function during CVB3-induced myocarditis and seems to be associated with an improved myocardial remodeling.

7. Activated factor X signaling via protease-activated receptor 2 suppresses pro-inflammatory cytokine production from lipopolysaccharide-stimulated myeloid cells.

8. Differential effects of murine and human factor X on adenovirus transduction via cell-surface heparan sulfate.

9. There was no detectable increase in plasma levels of mouse FX after active-site inhibited human APC administration to mice overexpressing human EPCR. FX does not effectively interact with EPCR in vivo, at least in regards to the mouse system.

10. investigation of role of F10a in progression of diabetic nephropathy: data from studies using inhibitor of F10a suggest that F10a does play a role in development of proteinemia, glomerular hypertrophy, and protein deposition in kidney of db/db mice

11. Data suggest that tissue factor and factor V induction by LPS may in part accelerate mesangioproliferative glomerulonephritis through activation of factor X and downstream proinflammatory and procoagulant mechanisms.

12. Gene targeting of tissue factor, factor X, and factor VII in mice: their involvement in embryonic development

13. Factor Xa functions in airway remodeling in asthma by stimulating mucin production, through regulation of amphiregulin expression and collagen deposition.

14. Complete absence of FX is incompatible with murine survival. Minimal FX activity as low as 1-3% is sufficient to rescue the lethal phenotype.

15. Results show that although factor Xa induces p42/44 MAP Kinase phosphorylation in endothelial cells, it has no direct effect on endothelial cell proliferation, protein synthesis and tube formation.

16. expression of coagulation factor X (FX) is locally increased in fibrotic lung tissue, with marked immunostaining associated with bronchial and alveolar epithelia

Cow (Bovine) Coagulation Factor X (F10) interaction partners

1. Identify potential phosphatidylserine-specific binding sites in the membrane binding domain of coagulation factor X.

2. Data suggest factor Xa (FXa) and factor Va (FVa) compete to bind FXa on both PS model membranes and microparticles from activated platelets; this competition between dimerization/prothrombinase complex formation appears to regulate blood coagulation.

3. thrombin and factor Xa diffusion along the heparin molecule explains the effects of extended heparin chain lengths

4. Factor Xa (fXa), a key serine protease of the coagulation system, was used as a model enzyme to test the canonical conformation hypothesis.

Zebrafish Coagulation Factor X (F10) interaction partners

1. These findings as well as the prolonged survival of f10(-/-) mutants will enable us to expand our understanding of the molecular mechanisms of hemostasis, including a platform for screening variants of uncertain significance in patients with F10 deficiency and other coagulation disorders