ライフサイエンスコーパス: factor X

1 both the enzyme factor IXa and the substrate factor X.

2 of membrane-bound protein substrates such as factor X.

3 ally accelerate activation of factor VII and factor X.

4 icant fraction of uncarboxylated recombinant factor X.

5 Xa showed greater affinity for heparin than factor X.

6 ted A1 subunit of factor VIIIa compared with factor X.

7 the 337-372 peptide to factor Xa but not to factor X.

8 an interactive site for either factor IX or factor X.

9 imulating factor IXa-catalyzed activation of factor X.

10 ermal growth factor (EGF) domain of clotting Factor X.

11 ) cofactor factor VIII(a), and (3) substrate factor X.

12 ial hematologic responses had improvement in factor X.

13 ted the factor VIIIa-dependent activation of factor X.

14 oward the small substrate (except R147A) and factor X.

15 es toward both a small peptide substrate and factor X.

16 ites and had altered apparent affinities for factor X.

17 its physiological inhibitor AT and substrate factor X.

18 nts also had decreased apparent affinity for factor X.

19 ed the central atom to be pure Pt (occupancy factor, x = 1.00(3)), is fortuitously in agreement with

20 , we detected an up-regulation of regulatory factor X, 3 (Rfx3) gene, a sequence-specific DNA-binding

21 posttranscriptional increases in regulatory factor X 5 mRNA and protein expression in OAD mice, as w

22 to the 3'-untranslated region of regulatory factor X 5.

23 Factor X(a) (FX(a)) binding to factor V(a) (FV(a)) on pl

24 hrombinase" complex, traditionally viewed as factor X(a) (FX(a)) in complex with factor V(a) (FV(a))

25 Tightly associated factor V(a) (FVa) and factor X(a) (FXa) serve as the essential prothrombin-act

26 e fluorescence of active-site-labeled bovine factor X(a) also varied with C6PS concentration in a sig

27 er is to extend these observations to bovine factor X(a) and to demonstrate that they do reflect conf

28 ed with fragments from both human and bovine factor X(a) are consistent with a common hypothesis for

29 (PS), regulates the proteolytic activity of factor X(a) as well as the structure of prothrombin.

30 (C6PS) enhances the proteolytic activity of factor X(a) by 60-fold.

31 mply, but cannot demonstrate, a C6PS-induced factor X(a) conformational change.

32 of human prothrombin to thrombin (II(a)) by factor X(a) during blood coagulation requires proteolysi

33 tes whose occupancy in both human and bovine factor X(a) elicits different structural and functional

34 (a) or Pre2-F1.2) back to the active site of factor X(a) for rapid conversion to thrombin.

35 rly demonstrated that C6PS binding to bovine factor X(a) induces secondary structural changes.

36 nce of Ca(2+), meaning that PS regulation of factor X(a) involves linkage between widely separated pa

37 are interpreted in terms of a model in which factor X(a) is regulated by sequential occupancy of a pa

38 membranes regulate prothrombin activation by factor X(a) mainly via interaction of individual PS mole

39 We report here that C6PS binding to factor X(a) not only enhances the rate of activation but

40 Activation by human factor X(a) of human prothrombin was examined in the abs

41 Activation of prothrombin by factor X(a) requires proteolysis of two bonds and is com

42 he fluorescence of active-site-labeled human factor X(a) showed that two linked sites specifically re

43 It was necessary to invoke the existence of factor X(a) species containing different lipids at each

44 r V(a) is a cofactor for the serine protease factor X(a) that activates prothrombin to thrombin in th

45 FV(a)) is a cofactor for the serine protease factor X(a) that activates prothrombin to thrombin in th

46 e specificities of lipid regulatory sites on factor X(a) that affect the rate of factor X(a)-catalyze

47 the structural responses of human and bovine factor X(a) to C6PS binding are somewhat different.

48 X(a), (2) alter the substrate specificity of factor X(a) to favor the meizothrombin intermediate, and

49 H(2)-terminal fragment ligand from MV-uPA by factor X(a) treatment ablated the MV-uPA functional acti

50 e C6PS binding sites to different domains of factor X(a) using a combination of activity, circular di

51 C6PS induced a 70-fold increase in bovine factor X(a)'s autolytic activity, consistent with the 60

52 data suggest that PS membranes (1) regulate factor X(a), (2) alter the substrate specificity of fact

53 as catalyzed by the prothrombinase complex (factor X(a), enzyme; factor V(a) and phosphatidylserine

54 sites on factor X(a) that affect the rate of factor X(a)-catalyzed prothrombin activation.

55 e in proteolytic activity reported for human factor X(a).

56 e hyperbolic fashion, also as seen for human factor X(a).

57 atidylserine, C6PS, bind to human and bovine factor X(a).

58 interaction of individual PS molecules with factor X(a).

59 oes not influence the functional response of factor X(a).

60 e appears to be the lipid regulatory site of factor X(a).

61 on proteolytic and biosynthetic fragments of factor X(a).

62 son of the binding constants of prothrombin, factor X, activated factor VII, and activated protein C

63 The assembly of the factor X activating complex on the platelet surface requ

64 Activated platelets promote intrinsic factor X-activating complex assembly by presenting high

65 platelet surface and for the assembly of the factor X-activating complex on activated platelets.

66 actor IXa assembly within the membrane-bound factor X-activating complex.

67 PDI enhances factor VIIa-dependent substrate factor X activation 5-10-fold in the presence of wild-ty

68 actor VIIa-tissue factor complexes supported factor X activation and factor VII autoactivation with e

69 both factor X and Xa binding sites, limiting factor X activation and forcing the release of bound fac

70 ut as classical noncompetitive inhibition of factor X activation by active site-directed ligands.

71 nic substrate hydrolysis and the kinetics of factor X activation by factor IXa.

72 The chimeras were deficient in supporting factor X activation by factor VIIa due to decreased k(ca

73 s with phospholipase D enhanced the rates of factor X activation by factor VIIa in the presence of so

74 ve counterparts, and the chimera accelerated factor X activation by factor VIIa.

75 ular target for direct heparin inhibition of factor X activation by intrinsic tenase (factor IXa-fact

76 ubunit was severely impaired in potentiating factor X activation by IXa(R333Q) and by a helix replace

77 ISIS 2302 did not inhibit factor X activation by the factor IXa-phospholipid compl

78 ISIS 2302 demonstrated partial inhibition of factor X activation by the factor IXa-phospholipid compl

79 resence of 30% ethylene glycol, the level of factor X activation by the factor IXa-phospholipid compl

80 LMWH also inhibited factor X activation by the factor IXa-PL complex via a d

81 ndent antithrombotic properties and inhibits factor X activation by the intrinsic tenase complex (fac

82 strated hyperbolic, mixed-type inhibition of factor X activation by the intrinsic tenase complex.

83 To identify amino acids essential for factor X activation complex assembly, recombinant factor

84 ent activity that is greatly enhanced in the factor X activation complex.

85 the affinity of factor IXa for the intrinsic factor X activation complex.

86 DHG inhibited factor X activation in a noncompetitive manner (reduced

87 Intrinsic factor X activation is accelerated >10(7)-fold by assemb

88 esent steady-state models of prothrombin and factor X activation under flow showing that zymogen and

89 have previously been identified as affecting factor X activation, and the residues of MM4 are located

90 ctor for factor IXa during intrinsic pathway factor X activation.

91 R165A demonstrated a defective Vmax(app) for factor X activation.

92 n and as a cofactor for factor VIIa-mediated factor X activation.

93 ites masks the diffusion-limiting effects of factor X activation.

94 holine strongly synergize with PS to enhance factor X activation.

95 nocytes, apoptosis, platelet activation, and factor X activation; and has antioxidant properties.

96 Russell's viper venom factor X activator (RVV-X) triggers the cascade, which r

97 ication to homogeneity and activation by the factor X activator from Russell viper venom, the mutants

98 ection of either DrKIn-I or RVV-X (the venom factor X-activator) into ICR mice did not significantly

99 el, simultaneous binding isotherms of (125)I-factor X and (131)I-factor VIII(a) to activated platelet

100 II-specific transcription factors regulatory factor X and CIITA and were transcriptionally active.

101 II-specific transcription factors regulatory factor X and CIITA.

102 blood clotting, prothrombin time, as well as factor X and factor IX activation.

103 results indicate that the binding regions of factor X and factor Xa for A1 domain overlap and that bo

104 Here we show that the factor X and prothrombin propeptides do not increase red

105 ilar Km values were observed for recombinant factor X and R240A substrates.

106 ta), indicating that both proteases activate factor X and that the poor activity of zymogen rFIX/VII-

107 contains interactive sites for both zymogen factor X and the active enzyme, factor Xa.

108 botic drugs including GII/GIIIA antagonists, factor X and thrombin-inhibitors requires a more conserv

109 te that bovine lactadherin competes for both factor X and Xa binding sites, limiting factor X activat

110 ed unstable complexes with blood coagulation factor X and, because of that, transduced the liver and

111 factor-factor VIIa (TF-FVIIa) activation of factors X and IX through the formation of the TF-FVIIa-F

112 d protein C toward their natural substrates (factors X and Va, respectively) than did PS-containing l

113 m is now known to act by directly activating factor X, and a form of the clotting test is used in the

114 ts of active factors VIII (VIIIa), IX (IXa), factor X, and Ca2+.

115 olipoprotein E, immunoglobulin light chains, Factor X, and complement proteins (C5 and C5b-9 complex)

116 pendent on the activity of CIITA, regulatory factor X, and CTCF.

117 pffer cells and LSECs, the level of clotting factor X, and hepatocyte infectibility did not differ be

118 e of the C1 domain on factor VIII binding to factor X, and indicate that cooperation between the C1 a

119 to the factor IXa active site or addition of factor X, and reduced by selected mutations in the hepar

120 r IX/factor IXa binding site, the substrate, factor X, and the active cofactor, factor VIIIa, form a

121 and shows 61% overall homology to regulatory factor X, ankyrin repeat-containing protein.

122 4-fold to K(d) approximately 0.8-1.5 nM) and factor X ( approximately 25-50-fold to K(d) approximatel

123 When prothrombin and factor X are activated coincident with each other, compe

124 tion (factor X or prothrombin), two pools of factor X are secreted; one is uncarboxylated and a secon

125 factor further indicates that factor Xa and factor X are similarly oriented toward their respective

126 Translin and translin-associated factor-x are highly conserved in eukaroytes; they can fo

127 RNA(11F7t) binds equivalently to the zymogen factor X as well as derivatives lacking gamma-carboxyglu

128 The selective inhibition of only factor X association with TF(1-218) will spare the intri

129 r of transcription, activating transcription factor x (ATFx), as a novel Tax-binding protein.

130 A single specific and selective factor X binding site was expressed (1200 sites/platelet

131 a and factor VIIIa there are two independent factor X binding sites: (1) low affinity, high capacity

132 C terminus of A1 contributes to the K(m) for factor X binding to factor Xase, and this parameter is c

133 factor IXa (4 nM) and factor II (4 microM), factor X binds to 3-fold more platelet sites than procof

134 rd, elevated expression of the transcription factor X box-binding protein 1 (XBP1) in DC appears to p

135 The transcription factor X-box binding protein 1 (XBP-1) is an essential p

136 The transcription factor X-box binding protein 1 (XBP-1) is essential for

137 core unfolded protein response transcription factor X-box binding protein 1 (XBP1) in liver regenerat

138 that Abeta activates the ER stress response factor X-box binding protein 1 (XBP1) in transgenic flie

139 s mechanism is mediated by the transcription factor X-box binding protein 1 (XBP1).

140 icing of the mRNA encoding the transcription factor X-box binding protein 1 (XBP1).

141 nfolded protein response (UPR) transcription factor X-box binding protein-1 (Xbp1) in intestinal epit

142 One effector of the UPR is the transcription factor X-box binding protein-1 (XBP1), which is expresse

143 Cleavage of the transcription factor X-box protein 1 and transcriptional activation of

144 UPR components, including the transcription factor X-box-binding protein 1 (XBP1), is increased foll

145 The transcription factor X-box-binding protein-1 (XBP-1) plays an essentia

146 d ER proteins and activating a transcription factor, X-box-binding protein 1, through endonucleolytic

147 The transcription factor, X-box-binding protein-1 (XBP1), controls the dev

148 LMWH with significantly higher affinity than factor X by competition solution affinity analysis, and

149 ole of membrane binding in the activation of factor X by extrinsic tenase under flow conditions, we d

150 Binding to iC3b and factor X by I-less Mac-1 was inhibited by the function-b

151 could increase the fraction of carboxylated factor X by reducing the affinity of the propeptide for

152 of 11 microM and inhibits the activation of factor X by the factor VIIIa-IXa complex with a K(i) of

153 C(50) of 30 nM for proteolytic activation of factor X by the TF(1-218)-VIIa complex.

154 portant for efficient rates of activation of factor X by this membrane-bound enzyme/cofactor complex.

155 The activation of coagulation factor X by tissue factor (TF) and coagulation factor VI

156 The activation of factor X by VIIa/TF and the Xa-dependent inhibition of t

157 riginal approach was designed using a set of factor X chimeras carrying regions of factor IX.

158 l cells by BADrUL131 and the fusion-inducing factor X clinical human cytomegalovirus isolate but do n

159 ld-type in thrombin-induced thromboembolism, factor X coagulant protein-induced thrombosis, and endot

160 In the presence of factor X, cofactor inactivation was inhibited, due to a

161 a approximately 1.6-fold increase in Km for factor X compared with wild type.

162 The physiologic activator of factor X consists of a complex of factor IXa, factor VII

163 ylated but that the fraction of carboxylated factor X could be increased to 92% by coexpressing the r

164 lead to the amelioration of amyloid-related factor X deficiency.

165 Ten factor X-deficient patients received high-dose melphalan

166 ed by interfering with exosite binding using factor X derivatives that are expected to have limited o

167 pid can both enhance and inhibit the rate of factor X (F.X) activation.

168 Deficiency of factor X (F10) in humans is a rare bleeding disorder wit

169 ries selected against the immobilized tissue factor x Factor VIIa (TF x FVIIa) complex.

170 rs, the activation peptides of factor IX and factor X, factor VII activity and antigen, activated fac

171 et; K(d) approximately 9 nM) when the shared factor X/factor II site was blocked by excess factor II

172 f RFX4 (RFX4_v3), a member of the regulatory factor X family of winged helix transcription factors.

173 s infected with the TB40E or fusion-inducing factor X (FIX) HCMV strains.

174 dings show that intramolecular activation of factor X following the zymogen to protease transition no

175 a pool of membrane-bound protein substrate (factor X) for efficient catalysis, or alternatively if i

176 regulatory element binding protein/Max-like factor X function.

177 d vesicles promote assembly of the intrinsic factor X (FX) activating complex by presenting high-affi

178 IXa (FIXa) are important for assembly of the factor X (FX) activating complex on phospholipid vesicle

179 n Ringhals cobra) that specifically inhibits factor X (FX) activation by the extrinsic tenase complex

180 Optimal rates of factor X (FX) activation require binding of factor IXa (

181 ctor VIIa (FVIIa)/tissue factor (TF)-induced factor X (FX) activation with an inhibitory concentratio

182 itor of TF x FVIIa, inhibiting activation of Factor X (FX) and Factor IX and amidolytic activity of C

183 enovirus (HAdv) interaction with coagulation factor X (FX) and introduced a mutation that abrogated f

184 Coagulation factor X (FX) binding to HAdV-5 mediates liver transduct

185 Recently, we demonstrated that coagulation factor X (FX) binds to Ad5-hexon protein at high affinit

186 ates the recognition and rapid activation of factor X (fX) by factor VIIa (fVIIa) in the extrinsic Xa

187 Once in the bloodstream, coagulation factor X (FX) has a pivotal role in determining Ad liver

188 ucture and dynamics of the human coagulation factor X (FX) have been investigated to understand the k

189 e demonstrated the importance of coagulation factor X (FX) in adenovirus (Ad) serotype 5-mediated liv

190 duction is mediated by the hexon-coagulation factor X (FX) interaction.

191 role in the coagulation cascade, coagulation factor X (FX) is involved in several major biological pr

192 Serum coagulation factor X (FX) is proposed to play a major role in adenov

193 pidermal growth factor-like (EGF1) domain in factor X (FX) or factor IX (FIX) plays an important role

194 ood coagulation, factor IXa (FIXa) activates factor X (FX) requiring Ca2+, phospholipid, and factor V

195 psid protein, hexon, binds human coagulation factor X (FX) with an affinity of 229 pM.

196 type 5 (Ad5) specifically binds coagulation factor X (FX), and FX is normally essential for intraven

197 mber I (SR-AI) as a receptor for coagulation factor X (FX), mediating the formation of an FX reservoi

198 with plasma proteins, including coagulation factor X (FX), which binds specifically to the major Ad5

199 e capsid hexon protein and blood coagulation factor X (FX), whilst penton-alpha(v)integrin interactio

200 ) complex activates both factor IX (FIX) and factor X (FX).

201 Ad5 transduction requires blood coagulation factor X (FX); FX binds to the Ad5 capsid hexon protein

202 essential reversible inhibitor of activated factor X (FXa) and also inhibits the FVIIa-TF complex.

203 Considering that activated coagulation factor X (FXa) is homologous to thrombin in the catalyti

204 equent association with the enzyme activated factor X (FXa) to form the prothrombinase complex is a p

205 e protease inhibitor that inhibits activated factor X (FXa) via a slow-tight binding mechanism and ti

206 tor (TFPI) is a well-characterized activated factor X (FXa)-dependent inhibitor of TF-initiated coagu

207 I), accelerating the inhibition of activated factor X (FXa).

208 d 4 of 10 bound to the activated coagulation factor X (FXa).

209 ns of thrombin and the activated coagulation factor X (FXa).

210 ffectively inhibit the activity of activated factor X (FXa); however, neither inhibitor exhibits any

211 nt study, we show that activated coagulation factors X (FXa) or VII (FVIIa) directly affect HSV1 infe

212 a dampening of the activity of the activated factor X-generating complex.

213 me critical region 1, or hagfish coagulation factor X genes.

214 Trax (Translin-associated factor X) has been shown to interact with TB-RBP/Transli

215 regulatory element binding protein/Max-like factor X heterodimer.

216 a series of alphaMbeta2 ligands (fibrinogen, Factor X, iC3b, ICAM-1 (intercellular adhesion molecule-

217 The role of procoagulant factor X in a murine model of ovalbumin (OVA)-induced as

218 ate the binding of blood coagulation factor (Factor X) in vitro.

219 binding studies support the conclusion that factor X initially binds to a high-capacity, low-affinit

220 The results showed that factor IX and factor X interacted with the same TF region located prox

221 ty is linked to active site conformation and factor X interaction during enzyme assembly.

222 Furthermore, factor Xa but not factor X interacts with high affinity at this site via r

223 and factor VIIa's catalytic interaction with factor X involve different regions in the catalytic doma

224 ropeptide, when sufficient overproduction of factor X is achieved, there is still a significant fract

225 nduced dilutional effects, we find that when factor X is activated in isolation by surface-localized

226 The serine protease zymogen factor X is converted to its catalytically active form f

227 further that a large pool of membrane-bound factor X is not required to support sustained catalysis.

228 Zymogen factor X is synthesized and modified in the liver.

229 oston Medical Center, 32 patients (8.7%) had factor X levels below 50% of normal.

230 MS had significantly higher prothrombin and factor X levels than healthy donors, whereas levels were

231 , and all 4 experienced improvement in their factor X levels.

232 e heart and lungs that were rescued in a low-factor X (low-FX) mouse background, suggesting a FX-medi

233 ene homolog 1 (avian) (ETS1), MYC-associated factor X (MAX), and specificity protein 12 (SP1).

234 ofibromin 1 (NF1; n = 2); and MYC-associated factor X (MAX; n = 1), and with sporadic PPGLs (n = 33)

235 The finding that factor Xa and factor X may engage in similar, if not identical, molecu

236 requires the heterodimeric partner Max-like factor X (Mlx) to bind to ChoRE sequences.

237 y element-binding protein (ChREBP), MAX-like factor X (MLX), and hepatic nuclear factor-4alpha (HNF-4

238 rofibromatosis 1 (n = 1), and myc-associated factor X (n = 1) and sporadic patients (n = 15) were inv

239 Here we show that a novel chromatin factor, X non-disjunction factor 1 (xnd-1), is responsib

240 ivation, whereas the Arg150 mutant activated factor X normally both in the absence and presence of fa

241 ulatory element binding protein and Max-like factor X nuclear abundance and interfere with glucose-re

242 Acquired deficiency of factor X occurs in patients with systemic amyloid light-

243 We report here that the factor X of such a cell line was only 52% carboxylated b

244 approaches were used to determine effects of factor X on the asthmatic response in mice.

245 netic constants obtained by either titrating factor X or factor VIIIa on SFLLRN-activated platelets o

246 PCR failed to accelerate FVIIa activation of factor X or protease-activated receptors.

247 e sequence is directing gamma-carboxylation (factor X or prothrombin), two pools of factor X are secr

248 e anticoagulant protein c2 (NAPc2) to either factor X or Xa is a requisite step in the pathway for th

249 ts indicate that on average 85% of the total factor X produced with the prothrombin propeptide was fu

250 GATA-4 transactivates the factor X promoter 28-fold in transient transfection expe

251 nded to 3 additional cis elements within the factor X promoter.

252 vement over a system that employs the native factor X propeptide, with which on average only 32% of t

253 duced expression of the base excision repair factor X-ray cross-complementing group 1 (XRCC1) and bre

254 r completely blocks factor IXa activation of factor X regardless of the presence of factor VIIIa.

255 f RFX5, RFXAP, and RFX-B/ANK, the regulatory factor X (RFX) complex is an obligate transcription fact

256 clear factor Y (NF-Y) complex and regulatory factor X (RFX) complex proteins.

257 tory factor as the heterotrimeric regulatory factor X (RFX) complex, which regulates transcription of

258 s bind nuclear factor Y (NFY) and regulatory factor X (RFX) complexes.

259 The regulatory factor X (RFX) family of transcription factors is crucia

260 nd specifically enriched in islet Regulatory Factor X (RFX) footprints.

261 Regulatory factor X (RFX) proteins are transcription factors.

262 MS1 transcription is regulated by regulatory factor X (RFX) proteins.

263 ranscription factors that include regulatory factor X (RFX), class II transcriptional activator (CIIT

264 riptional control complex, called regulatory factor X (RFX), that regulates the expression of major h

265 transactivator and 3 subunits of regulatory factor X (RFX): RFX containing ankyrin repeats (RFXANK),

266 a "three-hit" (genetic load x environmental factor x sex) theory of autism may help explain the male

267 Xa R165A had a 65% reduction in the kcat for factor X, suggesting an additional effect on catalysis.

268 s governing the liver-specific expression of factor X, the proximal promoter of human factor X was pr

269 e show that disruption of this transition in factor X through mutagenesis (FXa(I16L) and FXa(V17A)) n

270 shared with prothrombin, which then presents factor X to a specific high-affinity site consisting of

271 Furthermore, binding of factor X to adenovirus serotype 5 enhances infection of

272 amyloidosis, presumably due to adsorption of factor X to amyloid fibrils.

273 ransitions which accompany the conversion of factor X to factor Xa.

274 Factor X transcript levels and factor Xa activity were i

275 nits of the endonuclease translin-associated factor X (TRAX) and six subunits of the nucleotide-bindi

276 Translin-associated factor X (TRAX) is the predominantly cytoplasmic binding

277 Translin-associated factor X (TRAX) was identified as a protein that interac

278 e RNA processing protein translin-associated factor X (TRAX) with nanomolar affinity and that this bi

279 rtner protein of TB-RBP, Translin-associated factor X (TRAX), was absent in TB-RBP-deficient MEFs, de

280 ild-type TB-RBP and with Translin associated factor X (Trax).

281 the class II trans-activator and regulatory factor X, two transcription factors dedicated to major h

282 of X-isomers of vascular endothelial growth factor (X-VEGF).

283 ence and propeptide followed by mature human factor X was generated and stably transfected into HEK 2

284 Factor X was highly expressed in bronchoalveolar lavage

285 of factor X, the proximal promoter of human factor X was previously characterized.

286 transfected into HEK 293 cells, and modified factor X was purified from conditioned medium.

287 and -interacting protein Translin-associated factor X was reduced to 50% normal levels in heterozygot

288 d in part from a 5-fold increase in K(m) for factor X when A1 was cleaved at Arg(336).

289 in-Phe-Phe-Arg-factor IXa in the presence of factor X, whereas thrombin-cleaved HC yielded a marked i

290 ta binding partner TRAX (translin-associated factor X), which promotes RNA-induced gene silencing.

291 ternatively if it could efficiently activate factor X, which binds directly to the membrane nanodomai

292 The regulatory factor X with ankyrin repeats (RFXANK) is a subunit of a

293 dies revealed that the FIXa mutant activates factor X with approximately 4-fold decreased k(cat) and

294 e important for the interaction of substrate factor X with the tissue factor.factor VIIa complex.

295 ctivated monocytes more efficiently activate factor X with wound supernatant TF/factor VII(VIIa) comp

296 Activation of substrate factor X (X) by the TF--VIIa complex is here shown to pr

297 ell as drugs that directly inhibit activated factor X (Xa), which is the first protein in the final c

298 idermal growth factor-like domain (EGF-N) of factor X/Xa (FX/Xa) was investigated by constructing an

299 Production of recombinant factor X/Xa has proven to be difficult because of ineffi

300 However, the presence of factor X yielded minimal increases in anisotropy observe