1997
DOI: 10.1074/jbc.272.18.11863
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Abstract: Recent studies showed that the administration of active site-inhibited factor VIIa blocked factor VIIa/tissue factor-induced fibrin and thrombus formation in ex vivo and in vivo model systems. These studies suggest that inactivated factor VIIa competes efficiently with plasma factor VII(a) for a limited number of tissue factor sites. In the present study, we compared the interactions of factor VIIa and active site-inhibited factor VIIa with tissue factor. Competition studies of factor VIIa and active site-inhi… Show more

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Cited by 135 publications
(152 citation statements)
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“…The WT-FVIIai concentrations required to reach 50% inhibition (FVIIai⅐TF/FVIIa⅐TF ϭ 1.0) are reported in Table I. In agreement with the higher affinity of WT-FVIIai for TF (15,24,25), its concentration at 50% inhibition was lower than that of WT-FVIIa.…”
Section: Enhancement Of the Gla Domain Of Human Factor VIIsupporting
confidence: 48%
“…The WT-FVIIai concentrations required to reach 50% inhibition (FVIIai⅐TF/FVIIa⅐TF ϭ 1.0) are reported in Table I. In agreement with the higher affinity of WT-FVIIai for TF (15,24,25), its concentration at 50% inhibition was lower than that of WT-FVIIa.…”
Section: Enhancement Of the Gla Domain Of Human Factor VIIsupporting
confidence: 48%
“…FFR-FVIIa was prepared as described (21). Human thrombin, human FX and FXa were from Enzyme Research Laboratory Inc. (Lafayette, IN).…”
Section: Methodsmentioning
confidence: 99%
“…Measurements of Cell Surface FVIIa Binding Capacity and FVIIamediated FX Activation-Surface-exposed TF on transfected BHK cells was determined by FVIIa-mediated FXa generation and measurement of 125 I-FVIIa binding as described previously (21). Curve-fitting to a one-binding-site model using the Grafit (Erithacus Software Limited) program was applied for determination of the maximal number, B max , of 125 I-FVIIa binding sites.…”
Section: Methodsmentioning
confidence: 99%
“…Recombinant FVIIai was prepared at Novo Nordisk, Gentofte, Denmark, as described previously (37). In brief, the active site of recombinant FVIIa was inactivated by incubation with the tripeptide D-Phe-L-Phe-L-Arg chloromethyl ketone which forms covalent bonds to the active sites His-193 and Ser-344, thereby blocking these.…”
Section: Drugmentioning
confidence: 99%
“…This agent inhibits the formation of functional TF/ FVIIa complexes by competing with native plasma FVII(a) for binding sites on TF. The formed complexes are catalytically inactive, thereby preventing generation of FXa and thrombin with subsequent fibrin precipitation (37). A high dose of rFVIIai (1 mg/kg), which previously was shown to prevent local thrombosis and re-stenosis, was used (28,38).…”
Section: Introductionmentioning
confidence: 99%