Human Coagulation factor XII(F12) ELISA kit

Code CSB-EL007918HU
Size 96T,5×96T,10×96T
See More Details 24T ELISA kits trial application
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Product Details

Target Name coagulation factor XII (Hageman factor)
Alternative Names Factor XII ELISA Kit; Beta factor XIIa part 1 ELISA Kit; Beta factor XIIa part 2 ELISA Kit; Coagulation factor XII ELISA Kit; Coagulation factor XIIa heavy chain ELISA Kit; Coagulation factor XIIa light chain ELISA Kit; F12 ELISA Kit; F12 deficiency ELISA Kit; FA12_HUMAN ELISA Kit; Factor XII deficiency ELISA Kit; HAE3 ELISA Kit; HAEX ELISA Kit; HAF ELISA Kit; HAF deficiency ELISA Kit; Hageman factor ELISA Kit
Abbreviation F12
Uniprot No. P00748
Species Homo sapiens (Human)
Sample Types serum, plasma, tissue homogenates
Detection Range 0.312 ng/mL-20 ng/mL
Sensitivity 0.078 ng/mL
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Blood Coagulation
Assay Principle quantitative
Measurement Sandwich
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
To assess the linearity of the assay, samples were spiked with high concentrations of human F12 in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:1000Average %83
Range %80-86
1:2000Average %100
Range %97-103
1:4000Average %88
Range %84-92
1:8000Average %95
Range %90-100
The recovery of human F12 spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 9693-99
EDTA plasma (n=4)8885-91
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
202.592 2.573 2.583 2.441
102.318 2.309 2.314 2.172
51.737 1.746 1.742 1.600
2.51.125 1.168 1.147 1.005
1.250.679 0.698 0.689 0.547
0.6250.434 0.445 0.440 0.298
0.3120.291 0.275 0.283 0.141
00.141 0.143 0.142
and FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 7-14 working days

Target Data

Function Factor XII is a serum glycoprotein that participates in the initiation of blood coagulation, fibrinolysis, and the generation of bradykinin and angiotensin. Prekallikrein is cleaved by factor XII to form kallikrein, which then cleaves factor XII first to alpha-factor XIIa and then trypsin cleaves it to beta-factor XIIa. Alpha-factor XIIa activates factor XI to factor XIa.
Gene References into Functions
  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. Authors 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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Involvement in disease Factor XII deficiency (FA12D); Hereditary angioedema 3 (HAE3)
Subcellular Location Secreted
Protein Families Peptidase S1 family
Database Links

HGNC: 3530

OMIM: 234000

KEGG: hsa:2161

STRING: 9606.ENSP00000253496

UniGene: Hs.1321


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