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F11 encodes coagulation factor XI of the blood coagulation cascade. Additionally we are shipping Factor XI Antibodies (69) and Factor XI Proteins (15) and many more products for this protein.
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Data show that among the studied polymorphisms, only coagulation factor XI (F11) single nucleotide polymorphism rs2289252 was significantly associated with venous thrombosis (VT) and the F11 rs2289252-A allele was associated with a 1.6-fold increased risk of VT
Thus in conclusion, the bleeding manifestations in FXI deficiency are varied and unpredictable; neither correlates with FXI levels nor with the mutations. Comprehensive analysis of all the factors including both plasma and platelet FXI, global hemostatic factors like thrombin (show F2 ELISA Kits) generation potential may indicate a potential laboratory indicator for FXI deficiency related bleeding manifestations.
Fasudil reduced LPS (show IRF6 ELISA Kits)-mediated TF and PAI-1 (show SERPINE1 ELISA Kits) expression and activity in PBMCs. These effects may partially be relevant to the clinical benefits of fasudil in the treatment of CAPD patients.
High activity of factor XI indicates a risk of occurrence of deep vein thrombosis in post-trauma patients with fractures. F11 rs2089252 and rs2036914 (single nucleotide polymorphisms) are associated with activity of factors XI in such patients despite prophylaxis.
this study confirms the significant associations between polymorphism of 25264C.T in FXI and its activity and the risk of deep vein thrombosis after artificial joint replacement surgery
F11 genetic variants are associated with the risk of incident venous thrombosis among women
This study characterized FXI deficiency mutation spectrum in Chinese population with a high frequency of the W228*, G400V, Q263* and c.1136-4delGTTG mutations, which is distinct from that of other populations including Korean, Jewish or European populations.
F5 rs6025 and F11 rs2289252 contributed to the risk of recurrent venous thromboembolism and the combination is of potential clinical relevance for risk prediction
the co-localization of thrombin (show F2 ELISA Kits) and factor XI and the resultant efficient activation of FXI requires GPIb alpha (show GP1BA ELISA Kits)
factor XI is localized to GPIb in membrane rafts and that this association is important for promoting the activation of factor XI by thrombin (show F2 ELISA Kits) on the platelet surface
FXI attenuates part of the allergic response to repeated administration of house dust mite in the airways by a mechanism that is independent of activation via FXII (show F12 ELISA Kits).
Thrombin (show F2 ELISA Kits)-independent contribution of tissue factor (show F3 ELISA Kits) to inflammation and cardiac hypertrophy in a mouse model of sickle cell disease.
FXI deprivation was shown to slow down atherogenesis in Apoe (show APOE ELISA Kits) knockout mice.
anion-binding sites on FXIa that are required for expression of heparin's cofactor activity during protease inhibition by antithrombin (show SERPINC1 ELISA Kits) are also required for expression of polyP cofactor activity during FXI activation
Data conclude that within the mouse F11, Klkb1 (show KLKB1 ELISA Kits), Cyp4v3 (show CYP4V2 ELISA Kits) gene cluster, F11 and Cyp4v3 (show CYP4V2 ELISA Kits) frequently display striking parallel transcriptional responses suggesting the presence of shared regulatory elements.
Studies indicate that targeting factor XI (FXI) by knocking out the gene prevents arterial and vein thrombosis.
Protective roles for fibrin, tissue factor (show F3 ELISA Kits), plasminogen activator inhibitor-1 (show SERPINE1 ELISA Kits), and thrombin activatable fibrinolysis inhibitor (show CPB2 ELISA Kits), but not factor XI, during defense against the gram-negative bacterium Yersinia enterocolitica.
fXI and fXII (show F12 ELISA Kits) contribute to thrombus formation even when factor VIIa/tissue factor (show F3 ELISA Kits) initiates thrombosis.
Gene targeting of tissue factor (show F3 ELISA Kits), factor X, and factor VII (show TH ELISA Kits) in mice: their involvement in embryonic development
FXI is essential for thrombus formation following FeCl3-induced injury of the carotid artery in the mouse.
Sequence analysis of the bovine coagulation factor XI (F11) gene revealed an unusually high number of non-synonymous mutations. However, none of the mutations in the F11 gene were concordant with Bovine neonatal pancytopenia status.
Insertion of 15 nucleotides in the F11 gene is the causative mutation for factor XI deficiency in Japanese black cattle.
The molecular basis of coagulopathy has been recognized in Holstein cattle as a 76-bp insertion in the coding region of the FXI gene
This gene encodes coagulation factor XI of the blood coagulation cascade. This protein is present in plasma as a zymogen, which is a unique plasma coagulation enzyme because it exists as a homodimer consisting of two identical polypeptide chains linked by disulfide bonds. During activation of the plasma factor XI, an internal peptide bond is cleaved by factor XIIa (or XII) in each of the two chains, resulting in activated factor XIa, a serine protease composed of two heavy and two light chains held together by disulfide bonds. This activated plasma factor XI triggers the middle phase of the intrisic pathway of blood coagulation by activating factor IX. Defects in this factor lead to Rosenthal syndrome, a blood coagulation abnormality.
coagulation factor XI (plasma thromboplastin antecedent)
, platelet coagulation factor XI
, coagulation factor XI
, coagulation factor XI-like
, plasma thromboplastin antecedent
, factor XI
, blood coagulation factor XI