Recombinant Human Coagulation factor XII (F12), partial

1. Heterozygous F12 mutation decreases the plasma FXII activity approximately by half and cause moderate FXII deficiency in a Chinese population. PMID: 29587641
2. High levels of FXII activity are present in the plasma of multiple sclerosis patients during relapse. PMID: 27188843
3. defective FXII contact activation provides thromboprotection, excess activation underlies the swelling disorder hereditary angioedema type III. This review provides an overview of the molecular basis of FXII contact activation and FXII contact activation-associated disease states. PMID: 28346966
4. Accumulation of FXII in acute respiratory distress syndrome lungs may contribute to the release of pro-inflammatory mediators, regulating lung inflammation. PMID: 28816340
5. Data suggest that coagulation factor XII (FXII) homozygous p.Gly341Arg mutation, caused by consanguineous marriage, probably underlies the congenital FXII deficiency in the pedigree. PMID: 29419864
6. FXII deficiency impairs thrombosis in animal models without inducing abnormal excessive bleeding. Recent work has established the FXIIa-driven contact system as promising target for anticoagulant and anti-inflammatory drugs. This review focuses on the biochemistry of the contact system, its regulation by endogenous and exogenous inhibitors, and roles in disease states PMID: 28743596
7. Results demonstrated that the composition of the solution and the surface properties of the material all contribute to the observation of contact activation, and the activation of FXII is not specific to anionic surfaces as has been long believed. PMID: 28514863
8. Report an independent association between FXII levels and the risk of hemorrhagic stroke in Swedish population. PMID: 28433996
9. analysis of how FXII reacts to surface materials, which can be applied to the activities of FXII in its natural environment [review] PMID: 27282310
10. beta-amyloid interacts with fibrinogen and factor XII. These interactions can lead to increased clotting, abnormal clot formation, persistent fibrin deposition, and generation of proinflammatory molecules. PMID: 28661939
11. Abeta activates FXII, resulting in FXI activation and thrombin generation in human plasma, thereby establishing Abeta as a possible driver of prothrombotic states PMID: 26613657
12. results support a model for induction of contact activation in which activity intrinsic to single-chain FXII initiates alphaFXIIa and alpha-kallikrein formation on a surface. alphaFXIIa, with support from alpha-kallikrein, subsequently accelerates contact activation and is responsible for the full procoagulant activity of FXII. PMID: 28069606
13. The XPNPEP2 c-2399A and the ACE insertion/deletion polymorphisms analyzed in a population of patients with hereditary angioedema with F12 mutation were not a major determinant of disease expression. PMID: 27788882
14. in the presence of platelet polyphosphate and the downstream substrate fibrin, alphaFXIIa is a highly efficient and favorable plasminogen activator. PMID: 27694320
15. 6 different mutations, including 3 missense mutations (Gly341Arg, Glu502Lys and Gly542 Ser), 1 insertion (7142insertC) and 2 deletions (5741-5742 delCA and 6753-6755delACA), were identixFB01;ed on the F12 gene. Three of them (Gly341Arg, 5741-5742delCA and 6753-6755delACA) are reported here for the first time. PMID: 27003566
16. The present findings therefore suggest that homozygous FXII-HAE mutation status leads to a severe phenotype in females and males, and to an increased risk of manifest symptoms in the latter. PMID: 26392288
17. As the factor XII pathway specifically contributes to thrombosis but not to hemostasis, interference with this pathway provides a unique opportunity for safe anticoagulation that is not associated with excess bleeding. The review summarizes current knowledge on factor XII functions, activators and inhibitors. PMID: 25609114
18. It is concluded that F12-46C/T carriage acts as an independent modifier of hereditary angioedema due to C1-INH deficiency severity. PMID: 26248961
19. Active neutrophil extracellular traps formation can induce factor XII-mediated coagulation activation in patients with disseminated intravascular coagulation with poor prognosis. PMID: 26706311
20. findings suggest that the three mutations in the F12 gene are the causing reasons for the cross-reactive material-negative FXII deficiencies PMID: 26709783
21. Results report first report of FXii mutation causing angioedema in a Brazilian family with normal CI inhibitor status. PMID: 25816745
22. Results support the importance of contact activation pathway-dependent TG as a risk factor for ischemic stroke, and indicate the importance of F12 SNPs for TG ex vivo and in vivo. PMID: 26286125
23. Genotyping these subjects revealed that the carriers of the minor alleles at the two loci- F12 and KLKB1 had a significant association with reduced levels of active plasma renin. PMID: 26969407
24. The results provide an essential basis for the diagnosis of FXII deficiencies in Chinese. PMID: 26105808
25. We postulate that FXIIa first strengthens the clot structure during clot formation and thereafter contributes towards fibrinolysis. PMID: 26153047
26. Women with low FXII level might have an increased risk of premature delivery at < 34 GW. PMID: 25879167
27. Provide the structural basis for understanding FXII substrate recognition and zymogen activation. PMID: 25604127
28. data illustrate a critical role for polyphosphate/factor XII-triggered coagulation in prostate cancer-associated thrombosis with implications for anticoagulation without therapy-associated bleeding in malignancies PMID: 26153520
29. the results of this study characterize the mechanism of HAEIII and establish FXII inhibition as a potential therapeutic strategy to interfere with excessive vascular leakage in HAEIII PMID: 26193639
30. influence of FXII 46C/T on further pregnancy outcomes PMID: 25489738
31. Suggest C1-inh polymers activate the FXII-dependent kallikrein-kinin system in hereditary angioedema. PMID: 25800206
32. The heterozygous mutation of g.8597G>A identified in exon 13 of FXII gene is associated with hereditary coagulation factor XII deficiency. PMID: 26037346
33. an F12 mutation is the principal FXII-HAE predictor, with the disease expression influenced by individual variations in kinin degradation enzyme activities. PMID: 25134986
34. s report for the first time in Brazil a mutation in the F12 gene as a likely cause of HAE with normal C1-INH in patients with recurrent attacks of angioedema and/or abdominal pain. PMID: 25790805
35. In a cohort with hereditary angioedema, four families carried the p.Thr309Lys mutation in F12 gene. PMID: 25744496
36. Abeta42-mediated contact system activation is driven by factor XII and can occur in the AD circulation PMID: 25775543
37. Heparan sulfate enhances FXIIa binding capacity and consequently migration of human lung fibroblasts isolated from fibrotic lungs. PMID: 25589788
38. we identified the 72-bp F12 deletion in two Turkish women with hereditary angiodema-FXII. The mutation was located at the exon 9/intron 9 border and involved the proline-rich region of the factor XII protein (FXII. PMID: 25113305
39. FXIIa was increased three-fold in ESRD patients relative to control plasma. After conversion to nocturnal hemodialysis, both DeltaMAP and DeltaTPR correlated with DeltaFXIIa. PMID: 24733030
40. In hypercortisolemic patients, no significant disorders are present concerning FXII concentrations due to the C46T polymorphism of its gene promoter. PMID: 24691729
41. FVIIa- and FXIIa-triggered coagulation pathways have distinct but complementary roles in atherothrombus formation. PMID: 24855058
42. [review] As it forms, activated factor XII converts prekallikrein (PK) to kallikrein; kallikrein cleaves high-molecular-weight kininogen to release bradykinin. PMID: 24388213
43. Data suggest factor XII binding/autoactivation are increased on surface of hantavirus-infected vascular endothelium; thus, activation of kallikrein-kinin system during hantavirus infection could have profound implications on capillary permeability. PMID: 23874198
44. Generated a specific and potent FXII/FXIIa aptamer anticoagulant that offers targeted inhibition of discrete macromolecular interactions involved in the activation of the intrinsic pathway of blood coagulation. PMID: 23692437
45. Using different coagulation assays, it was shown that platelet contribution to whole blood coagulation was unrelated to the generation of activated FXII in vitro. PMID: 23896408
46. Mutation in the F12 gene is a prerequisite for the expression of hereditary angioedema disease symptoms, but other factors may have protective or aggravating effects on clinical features. PMID: 23849223
47. These results may confirm the importance of the proline-rich region of factor XII protein in edema formation PMID: 23994767
48. Immobilized Ni(2+) and Cu(2+) bind FXII, FXI and high molecular weight kininogen with high affinity and stimulate activation of the contact pathway, driving FXII-mediated coagulation. PMID: 22905925
49. the F12 46TT genotype is strongly associated with cerebral venous thrombosis in the south Indian population PMID: 22500857
50. The goal of this review is to summarize the in vivo functions of FXII, with special focus to its functions in thrombosis and vascular biology. PMID: 22993391

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HGNC: 3530

OMIM: 234000

KEGG: hsa:2161

STRING: 9606.ENSP00000253496

UniGene: Hs.1321