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F11 encodes coagulation factor XI of the blood coagulation cascade. Additionally we are shipping Factor XI Antibodies (86) and Factor XI Proteins (16) and many more products for this protein.
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FXI has a role in promoting a vascular coagulation-inflammatory circuit in arterial hypertension
thrombin activatable fibrinolysis inhibitor (show CPB2 ELISA Kits) pathway impairment, largely caused by a hitherto unknown TAFIa resistance, appears to be one main cause of decreased fibrinolytic resistance in FXI deficiency
Three loci showed robust, replicating association with circulating FXI levels: KNG1 (show KNG1 ELISA Kits) (rs710446, P-value = 2.07 x 10-302), F11 (rs4253417, P-value = 2.86 x 10-193), and a novel association in GCKR (show GCKR ELISA Kits) (rs780094, P-value = 3.56 x10-09), here for the first time implicated in FXI regulation. The two first SNPs (rs710446 and rs4253417) also associated with partial thromboplastin (show F3 ELISA Kits) time
The rs710446 and five low-frequency variant sets in KNG1 (show KNG1 ELISA Kits) with FXI level variation of Factor XI were significant after multiple testing correction and permutation.
Exploring the global landscape of genetic variation in coagulation factor XI deficiency
Structures of FXI in complex with the laminin-derived peptide EFPDFP and a DFP (show PPCS ELISA Kits) peptide from the random screen demonstrated binding in the same pocket, although in a slightly different conformation, thus revealing some flexibility in the molecular interactions of the FXI apple 2 domain.
inhibition of FXI and FXII (show F12 ELISA Kits) distinctly alter the biophysical properties of fibrin.
Acute Coronary Syndrome patients had an enhanced prothrombotic profile, demonstrated by an increased thrombin (show F2 ELISA Kits) generation potential, factor XIa and D-dimer levels.
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.
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