ライフサイエンスコーパス: factor VIIa

1 actor VIII, 10 nmol/L factor VII, 100 pmol/L factor VIIa).

2 ein cofactor for the plasma serine protease, factor VIIa.

3 e chimera accelerated factor X activation by factor VIIa.

4 ofound with a continuous, escalating dose of factor VIIa.

5 actor (TF), a cellular receptor for clotting factor VIIa.

6 actor Xa (FXa) generation in the presence of factor VIIa.

7 id binding and is required for activation by factor VIIa.

8 re only marginally influenced by addition of factor VIIa.

9 urface was substantially higher than that of factor VIIa.

10 -domain motions for FVII((IXegf1))a than for factor VIIa.

11 overall three-dimensional structure of human factor VIIa.

12 -100 pmol/L) circulates as the 2-chain form, factor VIIa.

13 size of the TF area that is in contact with factor VIIa.

14 vivo method for the continuous generation of Factor VIIa.

15 -initiated thrombin generation by 100 pmol/L factor VIIa.

16 X-ray crystal structure when complexed with factor VIIa.

17 he coagulant initiator complex tissue factor/factor VIIa.

18 be bypassed by administration of recombinant Factor VIIa.

19 ncies 1.5-fold and 2-fold lower than that of factor VIIa.

20 (FXa)-dependent inhibition of tissue factor/factor VIIa.

21 or continuous infusion of human recombinant factor VIIa (1 microg/kg per hour, n = 3).

22 The efficacy of factor VIIa (10-50 nM) in hemophilia blood is dependent

23 d over 8 hours after infusion of recombinant factor VIIa (15 ug/kg).

24 fter the live bacteria with site-inactivated Factor VIIa, a competitive tissue factor inhibitor, and

25 unique reagents for probing the mechanism of factor VIIa action.

26 gulation at multiple steps, including tissue factor VIIa activity, Xa activity, prothrombinase comple

27 Activated factor VIIa administration to adult and pediatric patien

28 E84C and T121C show that binding uninhibited Factor VIIa affects segmental motions in sTF.

29 h factor VIIa-tissue factor (TF) complex and factor VIIa alone initiated thrombin generation.

30 PA supported higher proteolytic activity by factor VIIa and activated protein C toward their natural

31 substantially more of two of these proteins, factor VIIa and activated protein C, than did equivalent

32 lso supported enhanced enzymatic activity of factor VIIa and activated protein C.

33 Recombinant factor VIIa and activated prothrombin complex concentrat

34 able differences exist in the trafficking of factor VIIa and active site-inhibited factor VIIa in fib

35 although a fraction of both the internalized factor VIIa and active site-inhibited factor VIIa recycl

36 At present, it is unknown whether factor VIIa and active site-inhibited factor VIIa underg

37 scent dyes were placed in the active site of factor VIIa and at the membrane surface.

38 equiring the use of bypassing agents such as factor VIIa and factor concentrates.

39 Exactin does not bind to the active site of factor VIIa and factor Xa based on its weak inhibition (

40 efined as active site-directed inhibitors of factor VIIa and factor Xa.

41 factor IX is activated to factor IXabeta by factor VIIa and factor XIa.

42 s of the solution structures of Ca(2+)-bound factor VIIa and FVII((IXegf1))a with tissue factor are p

43 athway inhibitor (TFPI), which inhibits both factor VIIa and its product, factor Xa.

44 tivated protein C; and group C (no binding), factor VIIa and kallikrein.

45 thrombin generation initiated by 100 pmol/L factor VIIa and low TF.

46 Furthermore, internalized factor VIIa and not active site-inhibited factor VIIa as

47 performance liquid chromatography, and both Factor VIIa and prothrombin fragment F1+2 were analyzed

48 f inhibition involving an activation loop of factor VIIa and represent a new framework for developing

49 molecular-weight heparins more potently than factor VIIa and shortened the bleeding time of mice trea

50 Tissue factor (TF) is a cofactor for factor VIIa and the primary cellular initiator of coagul

51 ne is associated with and may cause elevated Factor VIIa and thrombin generation in patients presenti

52 e extrinsic coagulation pathway, mediated by factor VIIa and tissue factor (TF), remains intact but i

53 Q333N fX is activated normally by factor VIIa and tissue factor, factors IXa and VIIIa, an

54 igh loss of function applied to PEG-modified factor VIIa and to active site-blocked blood clotting fa

55 r is the cell membrane-anchored cofactor for factor VIIa and triggers the coagulation reactions.

56 importance of PAR1 versus PAR2 in mediating factor VIIa and Xa responses, we assessed signaling in c

57 Factor VIIa and Xa-induced cellular migration was also i

58 VIIa and X, detected by digoxigenin-labeled factors VIIa and X, colocalized with TF protein in ather

59 In situ binding of TF to factors VIIa and X, detected by digoxigenin-labeled fact

60 prothrombin complex concentrate, recombinant factor VIIa, and epsilon-aminocaproic acid, as potential

61 iated factor Xa generation without exogenous factor VIIa, and TF activity was increased dramatically

62 x between tissue factor (TF) and coagulation factor VIIa, and two new receptors related to the class

63 een transfused; the early use of recombinant Factor VIIa; and, in military settings, the use of fresh

64 lant protein c2 (rNAPc2), an inhibitor of TF/factor VIIa, as a potential treatment.

65 evidence for the increased use of plasma and factor VIIa, as well as tourniquets, intraosseus devices

66 Factor VIIa associated with the nuclear fraction was int

67 ed factor VIIa and not active site-inhibited factor VIIa associates with nuclear fractions.

68 We tested this hypothesis by raising the factor VIIa binding site above the membrane surface by c

69 Factor VIIa binding to tissue factor on cell surfaces no

70 the catalytic activity increase caused when factor VIIa binds tissue factor.

71 ctive site-inhibited factor VIIa, similar to factor VIIa, binds to tissue factor on cell surfaces and

72 tive form factor Xa by the binary complex of factor VIIa bound to its cell surface receptor tissue fa

73 blood clotting, the plasma serine protease, factor VIIa, bound to the integral membrane protein, tis

74 posed of the trypsin-like serine proteinase, factor VIIa, bound to tissue factor (TF) on phospholipid

75 tion of thrombin, factor Xa, factor IXa, and factor VIIa by CDSO3, FDSO3, and SDSO3, three analogs of

76 Cleavage of factor VIIa by NN at Asp697 results in a cofactor that l

77 Once inside, the Factor VII is cleaved to Factor VIIa by the immobilized Factor Xa or XIIa.

78 actor Xa or XIIa, and continuously generates Factor VIIa bypass activity from the subject's own Facto

79 hrombin complex concentrates and recombinant factor VIIa can be used to reverse the effect of NOACs.

80 Thus, pharmacologic concentrations of factor VIIa cannot restore normal thrombin generation in

81 he mechanism by which tissue factor enhances factor VIIa catalytic activity.

82 Skeletal myosin supported factor VIIa cleavage of factor X equivalent to contamina

83 Factor VIIa cleaves these bonds sequentially, with accum

84 initiated by recombinant tissue factor (TF)-factor VIIa complex (5 pmol/L).

85 Inhibitors of the tissue factor (TF)/factor VIIa complex (TF-FVIIa) are promising novel antic

86 We examined whether the tissue factor/factor VIIa complex initiates the coagulation activation

87 Formation of the tissue factor-factor VIIa complex leads to the generation of thrombin

88 is initiated by formation of a tissue factor/factor VIIa complex on PS-exposed membranes and propagat

89 In fact, inhibition of the tissue factor/factor VIIa complex reduced mortality in a monkey model

90 Inhibition of the tissue factor-factor VIIa complex reduces coagulation and inflammation

91 2 is a potent inhibitor of the tissue factor/factor VIIa complex that has the potential to reduce isc

92 been derived by targeting the tissue factor-factor VIIa complex with naive peptide libraries display

93 activity (ie, activity of the tissue factor:factor VIIa complex) on human and rat smooth muscle cell

94 of substrate factor X with the tissue factor.factor VIIa complex.

95 nt binary complex inhibits the tissue factor-factor VIIa complex.

96 TFPI inhibition of both factor Xa and the TF/factor VIIa complex.

97 -expressed porcine tissue factor (pTF)-human factor VIIa complexes.

98 that are present in the human tissue factor-factor VIIa contact surface, suggesting a structural bas

99 he coagulation cascade, mediates coagulation factor VIIa-dependent activation of protease-activated r

100 in c2, a powerful inhibitor of tissue factor/factor VIIa-dependent coagulation (n = 6), or a control

101 TFPIalpha and TFPIbeta inhibit both TF-factor VIIa-dependent factor Xa (FXa) generation and fre

102 Tissue factor/factor VIIa-dependent pathway initiates coagulation acti

103 sed in E. coli, and their ability to support factor VIIa-dependent substrate activation was measured

104 We find that PDI enhances factor VIIa-dependent substrate factor X activation 5-10

105 owed 150-296-fold enhancement over wild-type factor VIIa, depending on the assay used.

106 The newly created Factor VIIa diffuses out of the chamber and back into th

107 ficient in supporting factor X activation by factor VIIa due to decreased k(cat).

108 s were used to probe the S2 pocket of tissue Factor VIIa enzyme to influence both potency and selecti

109 e S(1), S(2), and S(3) pockets of the tissue Factor VIIa enzyme.

110 e S(1), S(2), and S(3) pockets of the tissue Factor VIIa enzyme.

111 (AT-III)-mediated inactivation of IIa, mIIa, factor VIIa, factor IXa, and factor Xa; (c) the initial

112 substrate, in the absence of tissue factor, factor VIIa, factor VII(IXegf1)a, and K79Ra had similar

113 Thrombin, Factor VIIa, Factor Xa, and activated protein C were not

114 VII is consistent with its competition with factor VIIa for TF.

115 Although factor VII/factor VIIa (FVII/FVIIa) is known to interact with many

116 etween the trypsin-like protease coagulation factor VIIa (FVIIa) and its cofactor tissue factor (TF),

117 We recently showed that clotting factor VIIa (FVIIa) binding to endothelial cell protein

118 lation is triggered when the serine protease factor VIIa (fVIIa) binds to cell surface tissue factor

119 Recent studies have established that factor VIIa (FVIIa) binds to the endothelial cell protei

120 Recent studies have shown that factor VIIa (FVIIa) binds to the endothelial cell protei

121 The amidolytic activity of the TF.factor VIIa (FVIIa) complex toward a fluorogenic substra

122 t preventing initiation of coagulation at TF-Factor VIIa (FVIIa) complex would block fibrin depositio

123 itors specific for either tissue factor (TF)/factor VIIa (fVIIa) complexes or factor Xa (fXa) for ant

124 Factor VIIa (FVIIa) consists of a gamma-carboxyglutamic

125 Here we demonstrate that coagulation factor VIIa (FVIIa) elicits TF cytoplasmic domain-depend

126 A new series of peptide inhibitors of human Factor VIIa (FVIIa) has been identified and affinity mat

127 xosite on the protease domain of coagulation Factor VIIa (FVIIa) has been identified.

128 The serine protease factor VIIa (FVIIa) in complex with its cellular cofacto

129 ion and rapid activation of factor X (fX) by factor VIIa (fVIIa) in the extrinsic Xase pathway.

130 Factor VIIa (FVIIa) is a trypsin-like protease that play

131 e factor (TF) and the plasma serine protease factor VIIa (FVIIa) mediates the initiation of blood coa

132 Factor VIIa (FVIIa) or activated protein C binding to EP

133 its cofactor tissue factor (TF), coagulation factor VIIa (FVIIa) predominantly exists in a zymogen-li

134 act on coagulation, but potently inhibits TF/Factor VIIa (FVIIa) signaling through PAR2, inhibited aP

135 is an integral membrane protein cofactor for factor VIIa (fVIIa) that initiates the blood coagulation

136 Tissue factor (TF) binds the serine protease factor VIIa (FVIIa) to form a proteolytically active com

137 e presence of tissue factor is essential for factor VIIa (FVIIa) to reach its full catalytic potentia

138 Recombinant factor VIIa (FVIIa) variants with increased activity off

139 xtracellular interactions of plasma clotting factor VIIa (FVIIa) with tissue factor (TF) on cell surf

140 The complex of coagulation factor VIIa (FVIIa), a trypsin-like serine protease, and

141 r (TF) is the cellular receptor for clotting factor VIIa (FVIIa), and the formation of TF-FVIIa compl

142 is the cellular receptor for plasma protease factor VIIa (FVIIa), and the TF-FVIIa complex initiates

143 issue factor (TF), the cellular receptor for factor VIIa (FVIIa), besides initiating blood coagulatio

144 ncludes a step in which the soluble protein, factor VIIa (fVIIa), complexes with its transmembrane re

145 to protein C, activated protein C, plasmin, factor VIIa (FVIIa), FIX, FIXa, and FXII.

146 ential cofactor for the coagulation protease factor VIIa (FVIIa), initiating the coagulation cascade.

147 duce intracellular signaling in complex with factor VIIa (FVIIa).

148 ), the cellular receptor for plasma clotting factor VIIa (FVIIa).

149 rug-linker-Phe-Phe-Arg-methylketone (FFR-mk)-factor VIIa (fVIIa).

150 r (TF) is the cellular receptor for clotting factor VIIa (FVIIa).

151 pressed in insect cells and shown to inhibit factor VIIa (FVIIa)/tissue factor (TF)-induced factor X

152 y inhibitor-2 inhibits trypsin, plasmin, and factor VIIa (FVIIa)/tissue factor with Ki values of 13,

153 e initiation of coagulation by inhibition of Factor VIIa (FVIIa)/tissue factor/Factor Xa (FVIIa/TF/FX

154 Coagulation factors VIIa (FVIIa) and Xa (FXa) are proteases that act

155 Active site-inhibited blood clotting factor VIIa (fVIIai) binds to tissue factor (TF), a cell

156 Active site-inhibited factor VIIa (FVIIai) was obtained by inactivation with p

157 within the loop Lys159-Lys165, are near the factor VIIa gamma-carboxyglutamic acid (Gla) domain, sug

158 tamic acid (Gla) domain, suggesting that the factor VIIa Gla-domain may also participate in substrate

159 Animals treated with site inactivated Factor VIIa had less severe lung injury, with preserved

160 The catalytic domain of the chimeric factor VIIa has been disturbed and several surface loops

161 Recombinant factor VIIa has been increasingly used to provide hemost

162 ing of factor VIIa and active site-inhibited factor VIIa in fibroblasts.

163 Evidence so far indicates that the use of factor VIIa in hemophilic patients with inhibitors is bo

164 us recommendations on the use of recombinant factor VIIa in nonapproved settings have been developed,

165 Kunitz-1 binds and inhibits factor VIIa in the factor VIIa/tissue factor complex, an

166 lts suggest that the therapeutic efficacy of factor VIIa in the medical treatment of hemophiliacs wit

167 d DHPs studied is a potent inhibitor of free factor VIIa in the presence of antithrombin.

168 enhanced the rates of factor X activation by factor VIIa in the presence of soluble tissue factor.

169 warranted to establish the role of activated factor VIIa in the treatment of critically ill children.

170 and UAP (P=0.003), and modest elevations in Factor VIIa in UAP (P<0.05) compared with NCP but no dif

171 However, the short half-life of recombinant Factor VIIa in vivo negates its routine clinical use.

172 [PCC], activated PCC [aPCC], and recombinant factor VIIa) in the setting of TSOAC-associated bleeding

173 of this HBDt.TFt and its requisite cofactor (factor VIIa) in tumor models results in significant tumo

174 Factor VIIa, in complex with tissue factor (TF), is the

175 teins with egf1 residues changed to those in factor VIIa, including E51A, D64Q, FG74-75PA, and K79R.

176 for inhibiting thrombin over factor IXa and factor VIIa increased to 17-300-fold, suggesting a high

177 leading to the successful design of a potent factor VIIa inhibitor with a neutral lactam P1 and impro

178 h ultimately led to a 340 nM (IC(50)) tissue Factor VIIa inhibitor with selectivity over other relate

179 These compounds are thrombin, trypsin, and factor VIIa inhibitors and Choi is important for their b

180 or the pyrazinone core of noncovalent tissue Factor VIIa inhibitors and designed such that their subs

181 Targeted 2-pyridones were selected as tissue Factor VIIa inhibitors and prepared from 2,6-dibromopyri

182 uzuki coupling, afforded the targeted tissue Factor VIIa inhibitors.

183 Among the novel factor VIIa inhibitory fragments identified were aryl ha

184 Tissue factor, in association with factor VIIa, initiates the coagulation cascade.

185 for species specificity in the tissue factor-factor VIIa interaction.

186 Factor VIIa is also an important therapeutic agent for h

187 Coagulation factor VIIa is an allosterically regulated trypsin-like

188 The enzymatic activity of coagulation factor VIIa is controlled by its cellular cofactor tissu

189 Arg1545 and formation of the light chain of factor VIIa is essential for high affinity binding and f

190 Blood clotting factor VIIa is involved in the first step of the blood c

191 s hemophilia A model, approximately 2 nmol/L factor VIIa is needed to overcome the inhibition of phys

192 of factor XI (FXI) and/or tissue factor (TF)-factor VIIa, is essential for thrombosis and hemostasis.

193 ncts to damage control resuscitation such as factor VIIa may also be beneficial.

194 Recombinant factor VIIa may be used to reverse the effect of warfari

195 factor VII activation and as a cofactor for factor VIIa-mediated factor X activation.

196 Thus, factor VIIa mutants provided unique reagents for probing

197 rther studies revealed that, FX activated by factor VIIa on tissue factor bearing endothelial cells a

198 stepwise increase in F1+2 (P<0.0001) and of Factor VIIa (P<0.05).

199 lly diverse, neutral surrogates for cationic factor VIIa P1 groups, which are generally associated wi

200 In contrast, nonhematopoietic cell tissue factor-VIIa-PAR2 signaling specifically promoted obesity

201 insic (contact) and extrinsic (tissue factor/factor VIIa) pathways in the coagulation system, coagula

202 g was that PEG-modified, active site-blocked factor VIIa (PEG-VIIai, PEG-40 000) retained 40% of its

203 ia B blood in vitro, addition of 10 to 50 nM factor VIIa (pharmacologic concentrations) corrected the

204 d additional ligands for EPCR, which include factor VIIa, Plasmodium falciparum erythrocyte membrane

205 The structure of zebrafish factor VIIa predicted by homology modeling was consisten

206 r, they work by binding to an exosite on the factor VIIa protease domain, and non-competitively inhib

207 At 10 nmol/L, factor VIIa provided a thrombin generation response in t

208 ysteine and either F1+2 (r=-0.15, P=0.57) or Factor VIIa (r=0.22, P=0.37) in the NCP patients.

209 nd F1+2 (r=0.46, P<0.0001), homocysteine and Factor VIIa (r=0.24, P<0.01), and F1+2 and Factor VIIa (

210 d Factor VIIa (r=0.24, P<0.01), and F1+2 and Factor VIIa (r=0.41, P<0.0001).

211 e peptides do not bind to the active site of factor VIIa; rather, they work by binding to an exosite

212 alized factor VIIa and active site-inhibited factor VIIa recycle back to the cell surface, the amount

213 surface, the amount of active site-inhibited factor VIIa recycled back to the cell surface was substa

214 zed to position and align the active site of factor VIIa relative to the membrane surface for optimum

215 decisions about off-label use of recombinant factor VIIa remain at the physician's discretion, assist

216 Several questions pertaining to the use of factor VIIa require further investigation, including the

217 the solution structure of the light chain of factor VIIa (residues 1-142) in the absence of tissue fa

218 Thrombin activated factor Va (factor VIIa, residues 1-709 and 1546-2196) has an appare

219 of the catalytic domain, shifts relative to factor VIIa, resulting in a slight alteration of the act

220 The recent introduction of recombinant factor VIIa (rFVIIa) has been a welcome addition to the

221 Recombinant factor VIIa (rFVIIa) is approved for treatment of bleedi

222 Recombinant factor VIIa (rFVIIa) is used for treatment of hemophilia

223 (FDA) licensed recombinant human coagulation factor VIIa (rFVIIa) on March 25, 1999, for bleeding in

224 Recombinant factor VIIa (rFVIIa), a hemostatic agent approved for he

225 A new component therapy, recombinant factor VIIa (rFVIIa, NovoSeven), assists in turning on t

226 that factor VII activation by factor Xa and factor VIIa's catalytic interaction with factor X involv

227 We investigated factor VIIa's first epidermal growth factor-like (egf1)

228 del building was investigated using CDK2 and factor VIIa screening data sets.

229 Recombinant factor VIIa seems to have hemostatic effects in posttrau

230 Recombinant factor VIIa should be used with caution in cases with kn

231 tor in vivo reversed these effects of tissue factor-VIIa signaling and rapidly increased energy expen

232 Administration of coagulant factor VIIa significantly attenuated the DSS-induced col

233 Active site-inhibited factor VIIa, similar to factor VIIa, binds to tissue fac

234 dditional studies show that the internalized factor VIIa specifically associates with cytoskeletal pr

235 nt and TF signaling activities (responses to factor VIIa stimulation), and diminished TF emission as

236 cted against the immobilized tissue factor x Factor VIIa (TF x FVIIa) complex.

237 athway inhibitor (TFPI) blocks tissue factor-factor VIIa (TF-FVIIa) activation of factors X and IX th

238 oagulant protein that inhibits tissue factor-factor VIIa (TF-fVIIa) and factor Xa (fXa).

239 FPI) is the major inhibitor of tissue factor-factor VIIa (TF-FVIIa)-dependent FXa generation.

240 r of the clotting process, the tissue factor-factor VIIa (TF.FVIIa) complex.

241 f pyrazinone inhibitors of the Tissue Factor/Factor VIIa (TF/VIIa) complex.

242 mplex formation with its ligand, coagulation factor VIIa, TF influences protease-activated receptor-d

243 of factor VIIa was about 0.0001 that of the factor VIIa-TF complex.

244 as a competitive substrate with factor X for factor VIIa-TF.

245 ests that proteases generated as a result of factor VIIa/TF-mediated thrombin generation play a mecha

246 In contrast to factor VIIa, tissue factor is not found in the nuclear f

247 During physiologic clotting, the factor VIIa-tissue factor (FVIIa*TF) complex activates b

248 a (fXa)-dependent small protein inhibitor of factor VIIa-tissue factor (fVIIa.TF), which binds to a s

249 In normal blood, both factor VIIa-tissue factor (TF) complex and factor VIIa a

250 ow membrane microdomain composition controls factor VIIa-tissue factor activity, as reactions catalyz

251 Lactadherin also inhibited the factor VIIa-tissue factor complex efficiently whereas an

252 Factor VIIa-tissue factor complex formation initiates th

253 lity to function as a zymogen for either the factor VIIa-tissue factor complex or the factor IXa-fact

254 mplex with plasmin versus trypsin and/or the factor VIIa-tissue factor complex primarily due to stron

255 s wild-type tissue factor, and the resulting factor VIIa-tissue factor complexes supported factor X a

256 surrounding tissue factor by assembling the factor VIIa.tissue factor complex on stable bilayers con

257 shown that full proteolytic activity of the factor VIIa.tissue factor complex requires extremely hig

258 yer composition modulate the activity of the factor VIIa.tissue factor complex.

259 ctor IX (FIX) plays an important role in the factor VIIa/tissue factor (FVIIa/TF)-induced coagulation

260 Factor VIIa/tissue factor activity decrypted with methyl

261 plored the role of lipid rafts in regulating factor VIIa/tissue factor activity.

262 on phase assays measuring TFPI inhibition of factor VIIa/tissue factor catalytic activity, the rate o

263 manner, mediates feedback inhibition of the factor VIIa/tissue factor catalytic complex.

264 stallographic structure of human coagulation factor VIIa/tissue factor complex bound with calcium ion

265 nitz-1 binds and inhibits factor VIIa in the factor VIIa/tissue factor complex, and Kunitz-2 binds an

266 I contribute to thrombus formation even when factor VIIa/tissue factor initiates thrombosis.

267 insic" components initiated by factor XII or factor VIIa/tissue factor, respectively, and converging

268 s factor Xa-dependent feedback inhibition of factor VIIa/tissue factor-induced coagulation.

269 ot inhibit factor XIa, plasma kallikrein, or factor VIIa/tissue factor.

270 inhibits factor XIa, plasma kallikrein, and factor VIIa/tissue factor; accordingly, it has been prop

271 tissue factor (TF) binds the serine protease factor VIIa to activate coagulation or, alternatively, t

272 ion was considerably enhanced by addition of factor VIIa to both hemophilia A blood and "acquired" he

273 The ability of factor VIIa to initiate thrombin generation and clot for

274 the basis of a current clinical trial using factor VIIa to prevent rebleeding.

275 In vitro, this method generates sufficient Factor VIIa to substantially correct Factor VIII-deficie

276 and supported full allosteric activation of factor VIIa toward tripeptidyl-amide substrates.

277 hether factor VIIa and active site-inhibited factor VIIa undergo a similar intracellular processing.

278 s factor Xa (Xa) and the tissue factor (TF)--factor VIIa (VIIa) complex, but these enzymes are requir

279 The initiating coagulation protease factor VIIa (VIIa) differs by remaining in a zymogen-lik

280 e factor (TF), the receptor and cofactor for factor VIIa (VIIa) for cellular initiation of the coagul

281 ctor X by tissue factor (TF) and coagulation factor VIIa (VIIa) on a phospholipid surface is thought

282 Factor VIIa (VIIa) remains in a zymogen-like state follo

283 itiating protease of the coagulation system, factor VIIa (VIIa), retains zymogen-like features after

284 The efficiency of factor VIIa was about 0.0001 that of the factor VIIa-TF

285 Recombinant factor VIIa was initially developed for the treatment of

286 l structure of inhibitor 14a bound to tissue Factor VIIa was obtained and will be described.

287 That the active site of factor VIIa was raised above the membrane surface when b

288 Factor VII and factor VIIa were studied in a coagulation model using pl

289 tial step is the conversion of factor VII to factor VIIa which, in vitro, is efficiently catalyzed by

290 Factor VIIa, which also possesses Leu-8, bound soluble E

291 cascade exhibiting modest activity on tissue Factor VIIa with excellent selectivity over thrombin and

292 Starting with a factor VIIa with factor IX's egf1 domain (factor VII(IXe

293 The tissue factor/P-selectin chimeras bound factor VIIa with high affinity and supported full allost

294 TF binds factor VIIa with high affinity and, in addition, partici

295 ated that substitution of the EGF1 domain of factor VIIa with that of factor IX (FVII((IXegf1))a) res

296 ce via such metal-chelating lipids, it bound factor VIIa with the same high affinity as wild-type tis

297 platelets) completely convert factor VII to factor VIIa with wound pTF.

298 nt, reversible-covalent inhibitors of tissue Factor VIIa, with some analogues demonstrating selectivi

299 his study compared the activity of wild type factor VIIa (WT-VIIa) with that of a mutant with elevate

300 n activators), coagulation enzymes thrombin, factors VIIa, Xa, XIa, and XIIa, and activated protein C