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F10 encodes the vitamin K-dependent coagulation factor X of the blood coagulation cascade. De plus, nous expédions Coagulation Factor X Kits (51) et Coagulation Factor X Protéines (19) et beaucoup plus de produits pour cette protéine.
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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
PTX2 (Montrer PITX2 Anticorps) was identified PTX2 (Montrer PITX2 Anticorps) as a novel partner for FX, and both proteins cooperated to prevent their SR-AI (Montrer MSR1 Anticorps)-mediated uptake by macrophages.
annexin A2 (Montrer ANXA2 Anticorps) contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa.
Enhanced FXa and PAR2 (Montrer F2RL1 Anticorps) exacerbate DN and that both are promising targets for preventing diabetic nephropathy.
Macrophages regulate FX plasma levels in an SR-AI (Montrer MSR1 Anticorps)-dependent manner.
Factor Xa has a role in inhibiting HMGB1 (Montrer HMGB1 Anticorps)-induced septic responses in human umbilical vein endothelial cells and in mice
Selective inhibition of FXa improves the left ventricular function during CVB3-induced myocarditis and seems to be associated with an improved myocardial remodeling.
Activated factor X signaling via protease-activated receptor 2 (Montrer F2RL1 Anticorps) suppresses pro-inflammatory cytokine production from lipopolysaccharide-stimulated myeloid cells.
There was no detectable increase in plasma levels of mouse FX after active-site inhibited human APC (Montrer APC Anticorps) administration to mice overexpressing human EPCR (Montrer PROCR Anticorps). FX does not effectively interact with EPCR (Montrer PROCR Anticorps) in vivo, at least in regards to the mouse system.
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 (Montrer LEPR Anticorps) mice
Data suggest that tissue factor (Montrer F3 Anticorps) and factor V induction by LPS (Montrer TLR4 Anticorps) may in part accelerate mesangioproliferative glomerulonephritis through activation of factor X and downstream proinflammatory and procoagulant mechanisms.
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.
A coagulation initiating pathway is revealed in which the TF-FVIIa-nascent FXa complex activates FVIII (Montrer F8 Anticorps) apart from thrombin (Montrer F2 Anticorps) feedback.
Data suggest oxidized lipid vesicles with phosphatidylserine/polyunsaturated fatty acids promote inactivation of ZPI (Montrer SERPINA10 Anticorps)-PZ complex or free ZPI (Montrer SERPINA10 Anticorps); binding of PZ-complexed or free ZPI (Montrer SERPINA10 Anticorps) to oxidized vesicles mediates inactivation of ZPI (Montrer SERPINA10 Anticorps) (an inhibitor of FXa); blocking heparin- (anticoagulant-)binding site on ZPI (Montrer SERPINA10 Anticorps) interferes with binding to lipid or PZ. (ZPI (Montrer SERPINA10 Anticorps) = protein Z-dependent protease inhibitor (Montrer SERPINA10 Anticorps); PZ = protein Z (Montrer PROZ Anticorps); FXa = factor Xa)
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.
PTX2 (Montrer APCS Anticorps) was identified PTX2 (Montrer APCS Anticorps) as a novel partner for FX, and both proteins cooperated to prevent their SR-AI (Montrer MSR1 Anticorps)-mediated uptake by macrophages.
Individuals suffering from relapsing-remitting and secondary progressive multiple sclerosis had significantly higher prothrombin (Montrer F2 Anticorps) and factor X levels than healthy donors, whereas levels were unchanged in primary progressive MS and neuromyelitis optica patients.
Low concentrations of TF and exogenous FXIa, each too low to elicit a burst in thrombin (Montrer F2 Anticorps) production alone, act synergistically when in combination to cause substantial thrombin (Montrer F2 Anticorps) production.
analysis of how physiological concentrations of Tissue factor pathway inhibitor (Montrer TFPI Anticorps) inhibit FXa
According to our study, compounds 1a, 1g and 1s displayed evident FXa inhibitory activity and excellent selectivity over thrombin (Montrer F2 Anticorps) in in vitro inhibition activities studies.
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 (Montrer FGL2 Anticorps) complex formation appears to regulate blood coagulation.
thrombin (Montrer F2 Anticorps) and factor Xa diffusion along the heparin molecule explains the effects of extended heparin chain lengths
Factor Xa (fXa), a key serine protease (Montrer F2 Anticorps) of the coagulation system, was used as a model enzyme to test the canonical conformation hypothesis.
This gene encodes the vitamin K-dependent coagulation factor X of the blood coagulation cascade. This factor undergoes multiple processing steps before its preproprotein is converted to a mature two-chain form by the excision of the tripeptide RKR. Two chains of the factor are held together by 1 or more disulfide bonds\; the light chain contains 2 EGF-like domains, while the heavy chain contains the catalytic domain which is structurally homologous to those of the other hemostatic serine proteases. The mature factor is activated by the cleavage of the activation peptide by factor IXa (in the intrisic pathway), or by factor VIIa (in the extrinsic pathway). The activated factor then converts prothrombin to thrombin in the presence of factor Va, Ca+2, and phospholipid during blood clotting. Mutations of this gene result in factor X deficiency, a hemorrhagic condition of variable severity.
coagulation factor 10
, coagulation factor X
, vitamin K dependent serine protease
, coagulation factor X preproprotein
, Coagulation factor X
, stuart factor
, Stuart-Prower factor
, factor Xa
, blood coagulation factor X
, factor XA light chain
, virus activating protease
, virus-activating protease