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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 Anticorps (245) et Coagulation Factor X Protéines (33) et beaucoup plus de produits pour cette protéine.
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Mouse (Murine) Coagulation Factor X Kit ELISA pour Sandwich ELISA - ABIN2010768
Wang, Braun, Zhang, Norström, Thorlacius: Thrombin generation in abdominal sepsis is Rho-kinase-dependent. dans Biochemical and biophysical research communications 2015
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Mouse (Murine) Coagulation Factor X Kit ELISA pour Sandwich ELISA - ABIN424065
Wang, Braun, Zhang, Norström, Thorlacius: Monocytes regulate systemic coagulation and inflammation in abdominal sepsis. dans American journal of physiology. Heart and circulatory physiology 2015
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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.
this study demonstrated that thrombin and factor Xa cleavage sites on HEV pORF1 are obligatory for HEV replication.
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.
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 Kits ELISA) apart from thrombin (Montrer F2 Kits ELISA) feedback.
Data suggest oxidized lipid vesicles with phosphatidylserine/polyunsaturated fatty acids promote inactivation of ZPI (Montrer SERPINA10 Kits ELISA)-PZ complex or free ZPI (Montrer SERPINA10 Kits ELISA); binding of PZ-complexed or free ZPI (Montrer SERPINA10 Kits ELISA) to oxidized vesicles mediates inactivation of ZPI (Montrer SERPINA10 Kits ELISA) (an inhibitor of FXa); blocking heparin- (anticoagulant-)binding site on ZPI (Montrer SERPINA10 Kits ELISA) interferes with binding to lipid or PZ. (ZPI (Montrer SERPINA10 Kits ELISA) = protein Z-dependent protease inhibitor (Montrer SERPINA10 Kits ELISA); PZ = protein Z (Montrer PROZ Kits ELISA); 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 Kits ELISA) was identified PTX2 (Montrer APCS Kits ELISA) as a novel partner for FX, and both proteins cooperated to prevent their SR-AI (Montrer MSR1 Kits ELISA)-mediated uptake by macrophages.
annexin A2 (Montrer ANXA2 Kits ELISA) contributes to lung injury and fibrotic disease by mediating the fibrogenic actions of FXa.
Individuals suffering from relapsing-remitting and secondary progressive multiple sclerosis had significantly higher prothrombin (Montrer F2 Kits ELISA) and factor X levels than healthy donors, whereas levels were unchanged in primary progressive MS and neuromyelitis optica patients.
PTX2 (Montrer PITX2 Kits ELISA) was identified PTX2 (Montrer PITX2 Kits ELISA) as a novel partner for FX, and both proteins cooperated to prevent their SR-AI (Montrer MSR1 Kits ELISA)-mediated uptake by macrophages.
Enhanced FXa and PAR2 (Montrer F2RL1 Kits ELISA) exacerbate DN and that both are promising targets for preventing diabetic nephropathy.
Macrophages regulate FX plasma levels in an SR-AI (Montrer MSR1 Kits ELISA)-dependent manner.
Factor Xa has a role in inhibiting HMGB1 (Montrer HMGB1 Kits ELISA)-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 Kits ELISA) 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 Kits ELISA) administration to mice overexpressing human EPCR (Montrer PROCR Kits ELISA). FX does not effectively interact with EPCR (Montrer PROCR Kits ELISA) 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 Kits ELISA) mice
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.
Identify potential phosphatidylserine-specific binding sites in the membrane binding domain of coagulation factor X.
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 Kits ELISA) complex formation appears to regulate blood coagulation.
thrombin (Montrer F2 Kits ELISA) 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 Kits ELISA) of the coagulation system, was used as a model enzyme to test the canonical conformation hypothesis.
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
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.
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, factor XA light chain
, virus activating protease
, virus-activating protease
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, vitamin K dependent serine protease
, coagulation factor X preproprotein
, blood coagulation factor X
, Coagulation factor X
, coagulation factor 10 L homeolog