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Human F12 ELISA Kit for Sandwich ELISA - ABIN414549
Teligui, Dalmayrac, Corbeau, Bouquet, Godon, Denommé, Binuani, Verron, Boer, Baufreton: Ex vivo simulation of cardiopulmonary bypass with human blood for hemocompatibility testing. in Perfusion 2016
Active neutrophil extracellular traps formation can induce factor XII-mediated coagulation activation in patients with disseminated intravascular coagulation with poor prognosis.
findings suggest that the three mutations in the F12 gene are the causing reasons for the cross-reactive material-negative FXII deficiencies
Results report first report of FXii mutation causing angioedema in a Brazilian family with normal CI inhibitor status.
Factor XI and factor XII activities were significantly higher in patients with slow coronary flow than in controls, and could be associated with enhanced procoagulant state present in these patients.
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.
Genotyping these subjects revealed that the carriers of the minor alleles at the two loci- F12 and KLKB1 (show KLKB1 ELISA Kits) had a significant association with reduced levels of active plasma renin (show REN ELISA Kits).
The results provide an essential basis for the diagnosis of FXII deficiencies in Chinese.
We postulate that FXIIa first strengthens the clot structure during clot formation and thereafter contributes towards fibrinolysis.
Women with low FXII level might have an increased risk of premature delivery at < 34 GW.
Provide the structural basis for understanding FXII substrate recognition and zymogen activation.
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
Inhibiting factor XIIa with rHA-Infestin-4 may present a safe and effective treatment to decrease the morbidity of silent brain ischemia.
PKK (show RIPK4 ELISA Kits) or fXII deficiency reduced thrombus formation in both arterial and venous thrombosis models, without an apparent effect on hemostasis.
fXI (show F11 ELISA Kits) and fXII contribute to thrombus formation even when factor VIIa/tissue factor (show F3 ELISA Kits) initiates thrombosis.
F12 KNOCKOUT MICE, generated to elucidate the biological role(s) of FXII, had a markedly prolonged APTT. Deficiency of murine FXII does not cause thrombophilia or impaired fibrinolysis or affect hemostasis.
FXII-mediated fibrin formation is crucial for pathological arterial thrombosis but not for hemostasis
This gene encodes coagulation factor XII which circulates in blood as a zymogen. This single chain zymogen is converted to a two-chain serine protease with an heavy chain (alpha-factor XIIa) and a light chain. The heavy chain contains two fibronectin-type domains, two epidermal growth factor (EGF)-like domains, a kringle domain and a proline-rich domain, whereas the light chain contains only a catalytic domain. On activation, further cleavages takes place in the heavy chain, resulting in the production of beta-factor XIIa light chain and the alpha-factor XIIa light chain becomes beta-factor XIIa heavy chain. Prekallikrein is cleaved by factor XII to form kallikrein, which then cleaves factor XII first to alpha-factor XIIa and then to beta-factor XIIa. The active factor XIIa participates in the initiation of blood coagulation, fibrinolysis, and the generation of bradykinin and angiotensin. It activates coagulation factors VII and XI. Defects in this gene do not cause any clinical symptoms and the sole effect is that whole-blood clotting time is prolonged.
, beta-factor XIIa part 1
, beta-factor XIIa part 2
, coagulation factor XII
, coagulation factor XIIa heavy chain
, coagulation factor XIIa light chain
, factor XII
, hageman factor