anti-Coagulation Factor XI (F11) Antikörper

Human Coagulation Factor XI (F11) Interaktionspartner

1. Data indicate four new factor XI (FXI) gene defects potentially causing a functional deficiency and the duplication of 1653 bp involving exons 8 and 9.

2. In this prospective cohort of elderly adults, there was no statistically significant association of higher FXI levels with incident coronary heart disease and stroke.

3. Higher FIX antigen levels are associated with incident coronary heart disease in blacks but not in whites; the association of FXI levels with ischemic stroke is slightly attenuated after adjusting for stroke risk factors.

4. High molecular weight kininogen has an inhibitory effect on nucleic acid-supported fXI activation and may function as a negative regulator of fXI activation.

5. FXI has a role in promoting a vascular coagulation-inflammatory circuit in arterial hypertension

6. thrombin activatable fibrinolysis inhibitor (zeige CPB2 Antikörper) pathway impairment, largely caused by a hitherto unknown TAFIa resistance, appears to be one main cause of decreased fibrinolytic resistance in FXI deficiency

7. Three loci showed robust, replicating association with circulating FXI levels: KNG1 (zeige KNG1 Antikörper) (rs710446, P-value = 2.07 x 10-302), F11 (rs4253417, P-value = 2.86 x 10-193), and a novel association in GCKR (zeige GCKR Antikörper) (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 (zeige F3 Antikörper) time

8. The rs710446 and five low-frequency variant sets in KNG1 (zeige KNG1 Antikörper) with FXI level variation of Factor XI were significant after multiple testing correction and permutation.

9. Exploring the global landscape of genetic variation in coagulation factor XI deficiency

10. Structures of FXI in complex with the laminin-derived peptide EFPDFP and a DFP (zeige PPCS Antikörper) 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.

Cow (Bovine) Coagulation Factor XI (F11) Interaktionspartner

1. 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.

2. Insertion of 15 nucleotides in the F11 gene is the causative mutation for factor XI deficiency in Japanese black cattle.

3. The molecular basis of coagulopathy has been recognized in Holstein cattle as a 76-bp insertion in the coding region of the FXI gene

Mouse (Murine) Coagulation Factor XI (F11) Interaktionspartner

1. FXI(-/-) mice have a mild hemostatic defect after injury to the saphenous vein but not after transection of the tail or vessels in the abdominal wall.

2. FXI protects against sepsis derived from Streptococcus pneumoniae or Klebsiella pneumoniae pneumonia at least in part by enhancing the phagocytic capacity of neutrophils by a mechanism that is independent of activation via FXIIa.

3. 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 (zeige F12 Antikörper).

4. Thrombin (zeige F2 Antikörper)-independent contribution of tissue factor (zeige F3 Antikörper) to inflammation and cardiac hypertrophy in a mouse model of sickle cell disease.

5. FXI deprivation was shown to slow down atherogenesis in Apoe (zeige APOE Antikörper) knockout mice.

6. anion-binding sites on FXIa that are required for expression of heparin's cofactor activity during protease inhibition by antithrombin (zeige SERPINC1 Antikörper) are also required for expression of polyP cofactor activity during FXI activation

7. Data conclude that within the mouse F11, Klkb1 (zeige KLKB1 Antikörper), Cyp4v3 (zeige CYP4V2 Antikörper) gene cluster, F11 and Cyp4v3 (zeige CYP4V2 Antikörper) frequently display striking parallel transcriptional responses suggesting the presence of shared regulatory elements.

8. Studies indicate that targeting factor XI (FXI) by knocking out the gene prevents arterial and vein thrombosis.

9. Protective roles for fibrin, tissue factor (zeige F3 Antikörper), plasminogen activator inhibitor-1 (zeige SERPINE1 Antikörper), and thrombin activatable fibrinolysis inhibitor (zeige CPB2 Antikörper), but not factor XI, during defense against the gram-negative bacterium Yersinia enterocolitica.

10. fXI and fXII (zeige F12 Antikörper) contribute to thrombus formation even when factor VIIa/tissue factor (zeige F3 Antikörper) initiates thrombosis.