anti-Coagulation Factor X (F10) Antikörper

Human Coagulation Factor X (F10) Interaktionspartner

1. 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.

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

3. 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.

4. 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.

5. A coagulation initiating pathway is revealed in which the TF-FVIIa-nascent FXa complex activates FVIII (zeige F8 Antikörper) apart from thrombin (zeige F2 Antikörper) feedback.

6. Data suggest oxidized lipid vesicles with phosphatidylserine/polyunsaturated fatty acids promote inactivation of ZPI (zeige SERPINA10 Antikörper)-PZ complex or free ZPI (zeige SERPINA10 Antikörper); binding of PZ-complexed or free ZPI (zeige SERPINA10 Antikörper) to oxidized vesicles mediates inactivation of ZPI (zeige SERPINA10 Antikörper) (an inhibitor of FXa); blocking heparin- (anticoagulant-)binding site on ZPI (zeige SERPINA10 Antikörper) interferes with binding to lipid or PZ. (ZPI (zeige SERPINA10 Antikörper) = protein Z-dependent protease inhibitor (zeige SERPINA10 Antikörper); PZ = protein Z (zeige PROZ Antikörper); FXa = factor Xa)

7. 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.

8. PTX2 (zeige APCS Antikörper) was identified PTX2 (zeige APCS Antikörper) as a novel partner for FX, and both proteins cooperated to prevent their SR-AI (zeige MSR1 Antikörper)-mediated uptake by macrophages.

9. annexin A2 (zeige ANXA2 Antikörper) contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa.

10. Individuals suffering from relapsing-remitting and secondary progressive multiple sclerosis had significantly higher prothrombin (zeige F2 Antikörper) and factor X levels than healthy donors, whereas levels were unchanged in primary progressive MS and neuromyelitis optica patients.

Mouse (Murine) Coagulation Factor X (F10) Interaktionspartner

1. PTX2 (zeige PITX2 Antikörper) was identified PTX2 (zeige PITX2 Antikörper) as a novel partner for FX, and both proteins cooperated to prevent their SR-AI (zeige MSR1 Antikörper)-mediated uptake by macrophages.

2. annexin A2 (zeige ANXA2 Antikörper) contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa.

3. Enhanced FXa and PAR2 (zeige F2RL1 Antikörper) exacerbate DN and that both are promising targets for preventing diabetic nephropathy.

4. Macrophages regulate FX plasma levels in an SR-AI (zeige MSR1 Antikörper)-dependent manner.

5. Factor Xa has a role in inhibiting HMGB1 (zeige HMGB1 Antikörper)-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 (zeige F2RL1 Antikörper) suppresses pro-inflammatory cytokine production from lipopolysaccharide-stimulated myeloid cells.

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

9. 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 (zeige LEPR Antikörper) mice

10. Data suggest that tissue factor (zeige F3 Antikörper) and factor V induction by LPS (zeige TLR4 Antikörper) may in part accelerate mesangioproliferative glomerulonephritis through activation of factor X and downstream proinflammatory and procoagulant mechanisms.

Cow (Bovine) Coagulation Factor X (F10) Interaktionspartner

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 (zeige FGL2 Antikörper) complex formation appears to regulate blood coagulation.

3. thrombin (zeige F2 Antikörper) and factor Xa diffusion along the heparin molecule explains the effects of extended heparin chain lengths

4. Factor Xa (fXa), a key serine protease (zeige F2 Antikörper) of the coagulation system, was used as a model enzyme to test the canonical conformation hypothesis.

Zebrafish Coagulation Factor X (F10) Interaktionspartner

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