ライフサイエンスコーパス: factor VII

1 rexpression of tissue factor associated with factor VII.

2 genes were found for factor IX and four for factor VII.

3 tivated protein C resistance, hematocrit, or factor VII.

4 a protein with sequence similarity to human factor VII.

5 ifically involved in factor Xa activation of factor VII.

6 d 196 dizygotic twin pairs were analysed for factor VII.

7 to support factor Xa-mediated activation of factor VII.

8 plasma viscosity, von Willebrand factor, and factor VII.

9 me the inhibition of physiologic (10 nmol/L) factor VII.

10 centrations >100 pmol/L was not inhibited by factor VII.

11 about 20-fold higher than that of wild-type factor VII.

12 was 30 times greater than that of wild-type factor VII.

13 in time (PT) are known to have low levels of factor VII.

14 ermal growth factor-like domain with that of Factor VII.

15 that, after activation, cannot back-activate factor VII.

16 e Arg315-Lys316 peptide bond in intact F328S factor VII.

17 from UDP-glucose to an EGF repeat from human factor VII.

18 flow chamber, independent of factor XII and factor VII.

19 g of TF using an (18)F-labeled derivative of factor VII.

20 f-label utilization of recombinant activated factor VII.

21 Factor VII (10 nmol/L) extended the lag phase of thrombi

22 normal plasma, (100% factor VIII, 10 nmol/L factor VII, 100 pmol/L factor VIIa).

23 Combined analyses of the factor VII 10976A, GPIa 807T, GPIbalpha [-5]C, and GPIII

24 re raised mean platelet volume (4.0), raised factor VII (3.1), CP infection (2.7), previous mitral va

25 Sequencing of the patient's factor VII 5' flanking region, intron/exon junctions, an

26 lotting factor VII (VIIa) and the binding of factor VII(a) to TF initiates the coagulation cascade.

27 ed from the x-ray crystal coordinates of the factor VII(a)/tissue factor complex and oriented with th

28 tation evolves to a form different from both factors VII(a) and IX(a).

29 Deletion of the Habp2 gene encoding Factor VII-activating protease (FSAP) increases liver fi

30 Factor VII-activating protease (FSAP) is a circulating p

31 In this context, little is known about factor VII-activating protease (FSAP), which is activate

32 There is limited evidence that factor VII activation after a meal rich in polyunsaturat

33 al role-as a cofactor for factor Xa-mediated factor VII activation and as a cofactor for factor VIIa-

34 decreased relative to the rate of wild-type factor VII activation as revealed by densitometry scanni

35 is identified region, inhibited the rates of factor VII activation by 86% and 95%, respectively.

36 We conclude that factor VII activation by factor Xa and factor VIIa's cat

37 The rate of F328S factor VII activation by factor Xa was markedly decrease

38 observed Michaelis-Menten constants (KM) for factor VII activation in the presence of PCPS at optimal

39 In contrast, factor Va decreases the factor VII activation rate by factor Xa, reaching satura

40 medium-chain triacylglycerols do not induce factor VII activation.

41 d only one suggested changes consistent with factor VII activation.

42 conclude that the predominant physiological factor VII activator is, most likely, membrane-bound fac

43 Measured were plasma activated factor VII activity (FVIIa), FVII coagulant (FVIIC) acti

44 tivation peptides of factor IX and factor X, factor VII activity and antigen, activated factor XII, p

45 red by this treatment but prothrombin times, factor VII activity, prothrombin F-1 x 2 concentrations,

46 arily by high fibrinogen levels and elevated factor VII activity.

47 ), white blood cell (WBC) count, fibrinogen, factor VII, albumin, and hemoglobin-with subsequent elev

48 e important than dietary fat composition for factor VII and by implication its attendant risk of fata

49 n was assessed by measuring cleavage of 125I-factor VII and by the ability of unlabeled factor VII to

50 Factor VII and factor VIIa were studied in a coagulation

51 pTF preferentially accelerate activation of factor VII and factor X.

52 eved for clinically relevant loci within the factor VII and hemochromatosis genes.

53 rhage control, such as recombinant activated factor VII and hemostatic bandages, are in development.

54 ng enzyme (fVIIa) or zymogen (fVII) forms of factor VII and inhibits coagulation.

55 We conclude that factor VII and protein C bind preferentially to monoeste

56 We hypothesize that factor VII and protein C bind preferentially to the mono

57 sue factor (TF) expression, plasma F1.2, and factor VII and VIIa concentrations.

58 The concentrations of fibrinogen, factor VII and VIII, von Willebrand factor, plasminogen

59 ars to be distinct from the binding site for factors VII and VIIa as judged by a combination of biose

60 c activation steps that exist between TF and factors VII and VIIa; and (f) the activation of factor V

61 soluble plasma tissue factor (pTF) activate factors VII and X to generate thrombin.

62 latelets, pTF, and pTF fractions to activate factors VII and X were evaluated in pre-bypass, perfusat

63 onstants of prothrombin, factor X, activated factor VII, and activated protein C to seven different b

64 tes of three hemostatic factors--fibrinogen, factor VII, and factor VIII--were examined in the Cardio

65 hese MMPs did not cleave tissue factor (TF), factor VII, and factor Xa.

66 d HRT alters these, particularly fibrinogen, factor VII, and PAI (less change with transdermal HRT) a

67 nserved in prothrombin, factor IX, factor X, factor VII, and trypsin, is important for factor VIIa ca

68 proband has an extremely low plasma level of factor VII antigen and factor VII coagulant activity (<1

69 ct by which a high-fat diet increases plasma factor VII antigen concentration, and an acute effect wh

70 ntly across insulin quintiles, but levels of factor VII antigen, fibrinogen, and plasma viscosity did

71 iglycerides, C-reactive protein, fibrinogen, factor VII, apolipoproteins AI and B, lipoprotein-associ

72 f dietary enrichment with n-3 fatty acids on factor VII are uncertain.

73 resh-frozen plasma and recombinant-activated factor VII) are poorly aligned with recommended transfus

74 ich domain; GLA domain) of human coagulation factor VII as a test model.

75 ctor XIa (1 nM) are not observed to activate factor VII at detectable rates.

76 complexes supported factor X activation and factor VII autoactivation with essentially wild-type enz

77 eras fully supported tissue factor-dependent factor VII autoactivation.

78 eight velocity was inversely associated with factor VII (beta = -1.88, 95% CI: -3.84, 0.09), factor V

79 gulation inhibitors TFPI and AT-III present, factor VII both extended the lag phase of the reaction a

80 A relatively slow activation of factor VII bound to OC-2008 monolayers in the absence of

81 nts were performed to evaluate activation of factor VII bound to relipidated tissue factor (TF) in su

82 Autoactivation of factor VII bound to TF in suspension was dependent on th

83 n which helix 330-338 is replaced by that of factor VII) but it was normal for an epidermal growth fa

84 e venom's clotting activity does not require factor VII, but does require factor V and lipid.

85 In this study the activation of human factor VII by a variety of potential activators in the p

86 tors VII and VIIa; and (f) the activation of factor VII by IIa, factor Xa, and factor IXa.

87 Factor VII circulates as a single chain inactive zymogen

88 tprandial fibrinolytic activity and lipemia, factor VII coagulant (FVII:c) activity, and activated FV

89 The R353Q genotype is a major determinant of factor VII coagulant (FVIIc) activity, which is associat

90 y low plasma level of factor VII antigen and factor VII coagulant activity (<1 percent of normal) and

91 ibrinogen, activated factor XII (FXIIa), and factor VII coagulant activity (FVIIc) are associated wit

92 ) were 1.52, 1.35, and 1.15 (P:<0.0001); for factor VII coagulant activity (FVIIc, % standard), 114.5

93 rol concentrations (r = 0.48, P = 0.008) and factor VII coagulant activity (r = 0.46, P = 0.012) afte

94 ovel mutation in the F7 gene that results in factor VII coagulant activity (VII:c) of less than 1% an

95 ry fat intake is an important determinant of factor VII coagulant activity, a hemostatic risk factor

96 , TGF-beta(1), or fibrinogen concentrations; factor VII coagulant activity; or plasminogen activator

97 n, and active TGF-beta(1) concentrations and factor VII coagulant and plasminogen activator inhibitor

98 of factors VIIa, VIIc, and VIIag and TG, and factor VII codon 353 gene polymorphism.

99 in alpha (activated protein C) and activated factor VII concentrate (NovoSeven), have been used and m

100 ears to be located outside the tissue factor-factor VII contact zone.

101 Factor VII deficiency is a serious, potentially lethal d

102 re, recurrent hemorrhagic complications from factor VII deficiency, successfully treated with orthoto

103 ations have been identified in patients with factor VII deficiency, there have been no reports of mut

104 o brothers with severe inherited coagulation factor VII deficiency.

105 othrombin time), it was possible to diagnose factor VII deficiency.

106 HPCs expressed low levels of TF that clotted factor VII-deficient human plasma.

107 so revealed the formation of two novel F328S factor VII degradation products (40 and 9 kDa) resulting

108 Heterologous expression of zebrafish factor VII demonstrated a secreted protein (50 kDa) that

109 In addition, zebrafish factor VII demonstrates that the Gla-EGF-EGF-SP domain s

110 ng potential exists outside of the embryonic factor VII-dependent pathway.

111 pratherapeutic INR caused by parallel severe factor VII depletion.

112 Rapid fluctuations in factor VII during warfarin anticoagulation change the in

113 2 in the O-glucose consensus sequence ( ) of factor VII EGF repeat.

114 The Km values for factor VII EGF-1 domain and GDP-fucose are 15 and 6 micr

115 using the acceptor substrate, a recombinant factor VII EGF-1 domain, and the donor substrate analog,

116 recent phase II trial, recombinant activated factor VII (eptacog alfa) reduced haematoma expansion, m

117 hemophilia model (0% factor VIII, 10 nmol/L factor VII) equivalent to that observed with normal plas

118 studies indicate that the ETHYLENE RESPONSE FACTOR VII (ERF-VII) transcription factor is an importan

119 The ethylene response factor VII (ERF-VII) transcription factor RELATED TO APE

120 exerts a major positive regulatory effect on factor VII expression and provides in vivo evidence that

121 transcription factor is critical for normal factor VII expression.

122 n polymorphisms in the 5' promoter region of factor VII (F7), a coagulation factor, have been shown t

123 these associations are related to activated factor VII (factor VIIa).

124 pleiotropic relationships of F7 and F10 with Factor VII, Factor IX and cholesterol levels.

125 factors studied were prothrombin, activated factor VII, factor IX, factor X, activated protein C, pr

126 e propeptides (factor X, matrix Gla protein, factor VII, factor IX, PRGP1, and protein S) were betwee

127 6 hemostatic variables (D-dimer, fibrinogen, factor VII, factor VIIa, von Willebrand factor, and plas

128 of CVD with coagulation factors (fibrinogen, factor VII, factor VIII, and platelet aggregability) and

129 prothrombin, factor X, factor XI, factor IX, factor VII, factor VIII, factor V, protein C, protein S,

130 e variation in concentrations of fibrinogen, factor VII, factor VIII, PAI-1, tissue plasminogen activ

131 d against fibrinogen, prothrombin, factor V, factor VII, factor X, and von Willebrand factor, in whic

132 Although factor VII/factor VIIa (FVII/FVIIa) is known to interact

133 weight, and pack-years smoking, higher CRP, factor VII, fibrinogen, WBC count, and lower albumin and

134 Immunodepletion of factor VII from zebrafish plasma selectively inhibited t

135 we crossed mice doubly heterozygous for the factor VII (FVII(+/-)) and protein C (PC(+/-)) genes to

136 r-like domain (EGF-1) from blood coagulation factor VII (FVII) contains two unusual O-linked glycosyl

137 igated the mechanisms responsible for severe factor VII (FVII) deficiency in homozygous Italian patie

138 Factor VII (FVII) deficiency is a rare autosomal recessi

139 stigation of the molecular basis of a severe factor VII (fVII) deficiency revealed compound heterozyg

140 period in animal models of severe congenital factor VII (FVII) deficiency, a disease associated with

141 ly with homozygous lethal, blood coagulation factor VII (FVII) deficiency.

142 of activated factor VII (FVIIa) with zymogen factor VII (FVII) for tissue factor (TF) and loading of

143 Expression of the human coagulation factor VII (FVII) gene by hepatoma cells was modulated i

144 hether an additional loss of the coagulation factor VII (FVII) gene influenced the coagulopathy obser

145 er gene analysis of two regions of the human factor VII (FVII) gene promoter (residues -658 to -1 and

146 y the 5' sequences of the murine coagulation factor VII (fVII) gene that resulted in its efficient tr

147 T3 cells, and its efficiencies on generating Factor VII (FVII) gene-knockout (KO) mice.

148 experiments is used for studying the role of Factor VII (FVII) in venous thrombus formation.

149 Factor VII (FVII) is an important component of the coagu

150 Factor VII (FVII) is the natural ligand to TF.

151 g the F7 gene, were recently associated with factor VII (FVII) levels in European Americans (EAs).

152 Another targeting domain is factor VII (fVII), a zymogen that binds with high specif

153 Fibrinogen, coagulation factor VII (FVII), and factor VIII (FVIII) and its carri

154 stained for TF, TF-pathway inhibitor (TFPI), factor VII (FVII), and markers for endothelial cells (EC

155 IXa proteins using homologous sequences from factor VII (FVII): FIXa(FVIIEGF2) (FIX Delta 88-124,inve

156 mic acid domains of procoagulant coagulation factors VII (FVII) and X (FX).

157 Plasma levels of coagulation factors VII (FVII), VIII (FVIII), and von Willebrand fac

158 TF monoclonal antibody and activated factor VII (FVIIa) binding studies showed that little TF

159 ds, glucose, insulin, and activated clotting factor VII (FVIIa) concentrations.

160 nous infusion of recombinant human activated Factor VII (FVIIa) has been used for over a decade in th

161 Continuous expression of activated factor VII (FVIIa) via gene transfer is a potential ther

162 Catalytic domain variants of activated factor VII (FVIIa) with enhanced hemostatic properties a

163 Successful competition of activated factor VII (FVIIa) with zymogen factor VII (FVII) for ti

164 Ia) complex than with wound microparticle TF/factor VII(fVIIa).

165 on to factor V G1691A (ie, factor V Leiden), factor VII G10976A, prothrombin G20210A, plasminogen act

166 thrombosis (an arg353gln polymorphism in the factor VII gene and a T11053G polymorphism in the plasmi

167 tor VIIag and VIIc levels, are influenced by factor VII gene codon 353 polymorphism.

168 fied a point mutation in the promoter of the factor VII gene responsible for a severe bleeding disord

169 that correlated with an increase in hepatic Factor VII gene silencing of 28% (rHSA/siRNA) compared t

170 The human Factor VII gene spans 13 kilobase pairs and is located o

171 r VII promoter for in vivo expression of the factor VII gene.

172 It was evident that not all four factor VII genes are functional, essential active-site r

173 h a K(d) of 107 nm, whereas factor IX with a factor VII Gla domain (rFIX/VII-Gla) and factor IX expre

174 Recombinant activated factor VII has expanded available therapeutic options be

175 r neovasculature, presumably mediated by the factor VII immunoconjugate bound to tissue factor on neo

176 ascular endothelial cells and tumor cells, a factor VII immunoconjugate could be used for immunothera

177 nts showed that intratumoral delivery of the factor VII immunoconjugate, either alone or together wit

178 hibitory antibodies to TF and plasma lacking factor VII, implicating TF-dependent mechanisms.

179 safety and efficacy of recombinant activated factor VII in diverse clinical settings based on recent

180 We studied factor Xa activation of human factor VII in hopes of identifying factor VII residues,

181 l trials investigating recombinant activated factor VII in non-hemophiliacs have been published as ab

182 ibitors is, in part, based on overcoming the factor VII inhibitory effect.

183 rts would suggest that recombinant activated factor VII is an efficacious and safe "universal hemosta

184 Activated factor VII is approved for treating hemophilia patients

185 Once inside, the Factor VII is cleaved to Factor VIIa by the immobilized

186 The inhibition of factor Xa generation by factor VII is consistent with its competition with facto

187 n acute effect whereby a small proportion of factor VII is converted from its proenzyme to active ser

188 Identification of factor VII is critical in providing evidence for such a

189 Recombinant activated factor VII is increasingly being used for off-label trea

190 No detectable activation of 10 nM factor VII is observed under similar conditions when eit

191 Factor VII is the natural ligand to TF.

192 tamin K-dependent blood coagulation factors (factors VII, IX, and protein C) have become valuable pha

193 y similar to that of the coagulation-related factors VII, IX, and X and PC, but PZ differs from these

194 Factors VII, IX, and X play key roles in blood coagulati

195 binding sites in the homologous coagulation factors VII, IX, and X stabilize the structural orientat

196 ecular substrates (serine protease zymogens, factors VII, IX, and X).

197 ing epidermal growth factor domains, such as factors VII, IX, and X.

198 in structure, which is common to coagulation factors VII, IX, X, and protein C, was present before th

199 in whose structure is similar to coagulation factors VII, IX, X, protein C, and protein S, but whose

200 h factor X as substrate, due to higher Km's, factor VII(IXegf1)a and K79Ra had only 9% and 33% of fac

201 The Kd for factor VII(IXegf1)a binding to tissue factor was 60-200-

202 , in the absence of tissue factor, K79Ra and factor VII(IXegf1)a had catalytic efficiencies 1.5-fold

203 Only factor VII(IXegf1)a with the K79R (K79Ra) mutation, amon

204 With tissue factor, due to a kcat decrease, factor VII(IXegf1)a's catalytic efficiency (kcat/Km) was

205 a factor VIIa with factor IX's egf1 domain (factor VII(IXegf1)a), we made 4 proteins with egf1 resid

206 n the absence of tissue factor, factor VIIa, factor VII(IXegf1)a, and K79Ra had similar kcat's and Km

207 ntermediate between those of factor VIIa and factor VII(IXegf1)a.

208 inding with a Kd 3-8-fold lower than that of factor VII(IXegf1)a.

209 and insulin, RR interval, fibrinogen level, factor VII level and white blood cell and platelet count

210 Mean baseline factor VII levels dropped while on capecitabine therapy,

211 We investigated a girl with factor VII levels that were less than 1% of normal in as

212 yses compared changes in the PT and the PTT, factor VII levels, clinical hemostasis, blood component

213 is review suggest that activated recombinant factor VII may be a promising agent in the management of

214 Activated recombinant factor VII may be a therapy that is potentially useful i

215 es have suggested that activated recombinant factor VII may be useful in the management of some patie

216 ith standard PT-INR monitoring that includes factor VII measurement as well.

217 (icon) molecule, composed of a mutated mouse factor VII (mfVII) targeting domain and the Fc effector

218 The properties of a factor VII mutant, factor VII-Q10E32, relative to wild-t

219 in C deficiency, anticardiolipin antibodies, factor VII mutation, factor II mutation, and antiphospho

220 ated fatty acids, postprandial activation of factor VII occurs irrespective of the fatty acid composi

221 of MM4 are located at a hydrophobic patch of factor VII on the opposite side of the catalytic domain

222 rombin generation with recombinant activated factor VII or activated prothrombin complex concentrate

223 cascade by assembly with the serine protease factor VII or VIIa (VII/VIIa) resulting in formation of

224 ient in clotting plasma, although incubating factor VII or VIIa with the chimeras prior to the additi

225 the administration of activated recombinant factor VII, or determined the frequency of serious adver

226 sociation between SBP or DBP and fibrinogen, factor VII, or von Willebrand factor in either sex.

227 unt (P < 0.001), fibrinogen (P < 0.001), and factor VII (P < 0.001) levels and lower albumin (P < 0.0

228 orphisms in the genes coding for fibrinogen, factor VII, PAI-1, and factor XIII have been reported to

229 e patients who receive activated recombinant factor VII perioperatively.

230 en, plasma viscosity, von Willebrand factor, factor VII, plasminogen activator inhibitor antigen-1, a

231 Factor VII plays a pivotal role in coagulation.

232 patients with deficiencies of proconvertin (factor VII), proaccelerin (factor V), antihemophilic glo

233 ear factor 4 (HNF-4) binding site within the factor VII promoter (ACTTTG AE-->ACGTTG).

234 NF-4 was able to transactivate the wild-type factor VII promoter 5.4-fold in HeLa cells, no transacti

235 other nuclear proteins to this region of the factor VII promoter and resulted in a 20-fold reduction

236 erscore the importance of this region of the factor VII promoter for in vivo expression of the factor

237 ere have been no reports of mutations in the factor VII promoter.

238 sociation of coronary disease incidence with factor VII, protein C, antithrombin III, or platelet cou

239 Since plasma concentrations of prothrombin, factor VII, protein C, or protein S did not by themselve

240 hest affinity followed by the propeptides of factor VII, protein S, factor IX, protein C, and prothro

241 actor, tissue plasminogen activator antigen, factor VII, prothrombin fragment 1 + 2, urinary fibrinop

242 Because of its enhanced activity, factor VII-Q10E32 and its derivatives may provide import

243 le tissue factor and phospholipid, activated factor VII-Q10E32 displayed increased activation of fact

244 The properties of a factor VII mutant, factor VII-Q10E32, relative to wild-type factor VII (VII

245 17 men aged >52 y who were heterozygous for factor VII R353Q polymorphism were age-matched with subj

246 staining for activated caspase-3, rhodopsin, factor VII-related antigen and proliferating cell nuclea

247 of human factor VII in hopes of identifying factor VII residues, not adjacent to the cleavage site,

248 ve reported the use of recombinant-activated factor VII (rFVIIa) as an adjunct for reversal of coagul

249 Evidence suggests that recombinant activated factor VII (rFVIIa) can decrease intractable bleeding in

250 t to determine whether recombinant activated factor VII (rFVIIa) can reduce hematoma growth after int

251 Recombinant activated factor VII (rFVIIa) is a non-plasma-derived, rapid-actin

252 revious study in which recombinant activated factor VII (rFVIIa) reduced growth of the hematoma and i

253 ed the requirement for exogenous recombinant factor VII (rFVIIa) to approximately 20% of that before

254 safety and efficacy of recombinant activated factor VII (rFVIIa) used as the last resort for refracto

255 e antihemophilic agent recombinant activated factor VII (rFVIIa).

256 Recombinant activated human factor VII (rhFVIIa) is an established hemostatic agent

257 Infusion of recombinant activated human Factor VII (rhFVIIa), driving procoagulant reactions ind

258 dentified for eight serum proteins including Factor-VII[rs555212], Alpha-1-Antitrypsin[rs11846959], I

259 abstracts, supporting recombinant activated factor VII safety, but not its efficacy.

260 In the absence of factor VIII, factor VII significantly inhibits TF-initiated thrombin

261 Identification of zebrafish factor VII significantly narrows the evolutionary window

262 od coagulation caused by a defect in hepatic factor VII synthesis.

263 One targeting domain is factor VII that binds to tissue factor expressed on endo

264 se and C-reactive protein (CRP), fibrinogen, factor VII, tissue plasminogen activator (t-PA), LDL-C,

265 athway inhibitor-2 (TFPI-2), an inhibitor of Factor VII: tissue factor signal transduction known to d

266 I-factor VII and by the ability of unlabeled factor VII to catalyze activation of a variant factor IX

267 The initial step is the conversion of factor VII to factor VIIa which, in vitro, is efficientl

268 not activated platelets) completely convert factor VII to factor VIIa with wound pTF.

269 Recent trials of recombinant factor VII to slow initial bleeding are discussed.

270 The Nt-Cys ETHYLENE RESPONSE FACTOR VII transcription factor substrates enhance patho

271 In this report, we show that Factor VII transcripts are restricted to the liver and t

272 here it remains sequestered from circulating factor VII until vascular integrity is disrupted or unti

273 nt, factor VII-Q10E32, relative to wild-type factor VII (VII, containing P10K32), have been compared.

274 r receptor for an activated form of clotting factor VII (VIIa) and the binding of factor VII(a) to TF

275 Activated factor VII (VIIa) was measured in 829 men.

276 activate factor X with wound supernatant TF/factor VII(VIIa) complex than with wound microparticle T

277 ts such as tissue factor (TF) to circulating factor VII/VIIa (FVII/VIIa) lead to intravascular thromb

278 at localizes the coagulation serine protease factor VII/VIIa (FVII/VIIa) to the cell surface.

279 dies indicate that proper positioning of the factor VII/VIIa binding site on tissue factor above the

280 ylphosphoryl factor Xa and factor Xa but not factor VII/VIIa or prothrombin bound to immobilized VP31

281 laque disruption and exposure of circulating factor VII/VIIa to subendothelial procoagulants such as

282 F), a transmembrane receptor for coagulation factor VII/VIIa, is aberrantly expressed in human cancer

283 is related to tissue factor associated with factor VII/VIIa.

284 e plasminogen activator antigen, fibrinogen, factor VII, von Willebrand factor, fibrinogen, and plasm

285 ic efficiency of factor Xa for activation of factor VII was 176- and 234-fold higher than that for H1

286 rboxyglutamic acid domain) of blood clotting factor VII was carried out to identify sites that improv

287 recombinant human TF complexed to activated factor VII was inhibited by PAEC and HAEC-associated TFP

288 ature and on tumor cells; the active site of factor VII was mutated to inhibit the initiation of bloo

289 Factor VII was shown to be present in zebrafish blood an

290 Only subnanomolar amounts of factor VII were activated when prothrombin activation wa

291 r hemodilution, and ratios of factor VIIa to factor VII were highest in pericardial samples (P < .05)

292 Serum lipids and factor VII were measured in both studies.

293 n which helix 330-338 is replaced by that of factor VII) were expressed, purified, and characterized.

294 y inhibited the conversion of (125)I-labeled factor VII when cell membrane-expressed, full-length tis

295 VIIa bypass activity from the subject's own Factor VII, which enters the chamber by diffusion.

296 I) and activated (VIIa) forms of coagulation factor VII with high affinity.

297 44A, R147A, Y179A, D186A, and F256A) and two factor VIIs with multiple mutations [MM3 (L144A/R147A/D1

298 We made eight factor VIIs with single mutations (N100A, H101A, D102Q,

299 NR corresponded most closely with changes in factor VII, with a highly collinear relationship between

300 Individual variations in factors VII, XI, and X concentrations had little effect