ライフサイエンスコーパス: factor Xa

1 on potency and selectivity over thrombin and factor Xa.

2 1)s(-1)) and selectively (> 20-fold) inhibit factor Xa.

3 t platelet subpopulations capable of binding factor Xa.

4 h inhibits both factor VIIa and its product, factor Xa.

5 e was changed to permit activation by bovine factor Xa.

6 atorial library based on its ability to bind factor Xa.

7 ng cleavage and activation of prothrombin by factor Xa.

8 1 but does not enhance coagulant function of factor Xa.

9 antithrombin, thereby indirectly inhibiting factor Xa.

10 block the activation of fVIII by thrombin or factor Xa.

11 rotein, or protease activity of thrombin and Factor Xa.

12 ty related to an ability to bind and inhibit factor Xa.

13 , matrix metalloproteinase-9 (4.1-fold), and Factor Xa (3.8-fold)).

14 trate selectivity profile similar to that of factor Xa, a Na(+)-activated protease involved in blood

15 thelial cells and that annexin 2 facilitates factor Xa activation of PAR-1 but does not enhance coagu

16 ies several features of the hydration of the factor Xa active site relevant to the structure-activity

17 pH dependence indicative of participation of factor Xa active-site residues.

18 single type of AT-binding site and high anti-factor Xa activity (137 +/- 36 units/mg).

19 from baseline of 39% in the measure of anti-factor Xa activity among patients receiving rivaroxaban

20 re evaluated for changes in measures of anti-factor Xa activity and were assessed for clinical hemost

21 er the bolus administration, the median anti-factor Xa activity decreased by 89% (95% confidence inte

22 sion of andexanet substantially reduced anti-factor Xa activity in patients with acute major bleeding

23 of 47 patients had a baseline value for anti-factor Xa activity of at least 75 ng per milliliter (or

24 g the rivaroxaban-treated participants, anti-factor Xa activity was reduced by 92% among those who re

25 mong the apixaban-treated participants, anti-factor Xa activity was reduced by 94% among those who re

26 -terminal region of factor Va heavy chain to factor Xa activity within prothrombinase and demonstrate

27 outcome was the mean percent change in anti-factor Xa activity, which is a measure of factor Xa inhi

28 generated APC led to increased TF-dependent factor Xa activity.

29 Multiple direct anti-factor Xa agents are currently undergoing evaluation in

30 with anticoagulants that target thrombin or factor Xa alone.

31 With numerous novel factor Xa and direct thrombin inhibitor drugs completing

32 s from the ability of the aptamer to bind to factor Xa and exclude interactions between the proteinas

33 Factor Xa and factor IIa (thrombin) play roles in thromb

34 ion as exosites to promote the inhibition of factor Xa and factor IXa when the serpin is conformation

35 tially active prothrombinase complex between factor Xa and factor Va(2), compared with K(d)(app) for

36 100-fold accelerations of ZPI reactions with factor Xa and factor XIa to yield second order rate cons

37 ular-weight heparin: Potent activity against factor Xa and IIa, predictable pharmacokinetics after bo

38 Starting from compound 14, with low factor Xa and modest anti-thrombin inhibitory activities

39 red for the interaction of the cofactor with factor Xa and optimum rates of prothrombin cleavage.

40 methanol to multiple pockets on the proteins Factor Xa and p38 MAP kinase.

41 ral B domain which exposes binding sites for factor Xa and possibly prothrombin.

42 evealed that 16:0 acylcarnitine was bound to factor Xa and that binding did not require the gamma-car

43 ARC19499 blocks TFPI inhibition of both factor Xa and the TF/factor VIIa complex.

44 , which displays strong activity in vitro vs factor Xa and thrombin (with Ki's of 1 and 8 nM, respect

45 tithrombin independent (direct inhibitors of factor Xa and thrombin [factor IIa]).

46 tralized the heparin-catalyzed inhibition of factor Xa and thrombin by AT in a Zn(2+)-dependent manne

47 ersibly inactivates the clotting proteinases factor Xa and thrombin by forming covalent complexes wit

48 formation and markedly reduced generation of factor Xa and thrombin on platelets.

49 Antithrombin mainly inhibits factor Xa and thrombin.

50 al of the N-terminal domain by cleavage with factor Xa and treatment with KNO3 and MgATP did not, how

51 specificity of FXIIa and its close homologue factor Xa and used these data, together with inhibitor-b

52 agulant drug that inhibits the activities of factors Xa and IIa (also known as thrombin) to prevent b

53 constant for the reactions of alpha1PI with factors Xa and IXa 11-14-fold, comparable with their rat

54 ly activates antithrombin as an inhibitor of factors Xa and IXa by enhancing the initial Michaelis co

55 assive 10-200-fold losses in reactivity with factors Xa and IXa in both unactivated and heparin-activ

56 determinant of antithrombin reactivity with factors Xa and IXa in the native as well as the heparin-

57 e variants exhibited basal reactivities with factors Xa and IXa, heparin affinities and thermal stabi

58 was monitored using biolayer interferometry, factors Xa and Va each showed favorable binding interact

59 was bell-shaped for ZPI reactions with both factors Xa and XIa, consistent with a template-bridging

60 tor-dependent regulator of blood coagulation factors Xa and XIa.

61 Thrombin, Factor VIIa, Factor Xa, and activated protein C were not effective.

62 veloped that selectively inhibit thrombin or factor Xa, and have predictable dose-response relationsh

63 itor, enhances the inhibition of coagulation factor Xa, and protein Z-dependent protease inhibitor in

64 d not form stable complexes with thrombin or factor Xa, and the I207T/I207A variants inhibited both p

65 rate when enoxaparin sodium is dosed by anti-factor Xa (anti-Xa) trough level is not well described.

66 microscopy using a fluorophore-labeled anti-factor Xa antibody, which demonstrated the presence of d

67 coagulation enzymes thrombin (dabigatran) or factor Xa (apixaban, rivaroxaban, and edoxaban) and give

68 prolonged half-lives compared with wild-type factor Xa (approximately 60 minutes vs approximately 1 m

69 C6PE and C6PS binding sites of factor Xa are specific, distinct, and linked, because bi

70 Mutation of factor Xa Arg(143), Lys(148), and Arg(150) residues that

71 s complex interaction of alpha1PI with S195A factor Xa as they do with the heparin-activated antithro

72 or Xa, heparin activates ZPI to inhibit free factor Xa as well as factor XIa and therefore may play a

73 cific fluorescence detection of thrombin and factor Xa at only 500 fM concentration.

74 t bind to the active site of factor VIIa and factor Xa based on its weak inhibition (IC50 >> 300 muM)

75 n factors, with those targeting thrombin and factor Xa being most advanced in development.

76 dentified amino acids that are important for factor Xa binding (i.e., E (323)Y (324) and E (330)V (33

77 on of the p-methoxyphenyl P1, which retained factor Xa binding affinity and good oral bioavailability

78 ed thrombin markedly increases Annexin V and factor Xa binding to platelets, consistent with the form

79 Inhibition of factor Xa by acylcarnitines was greater for longer acyl

80 consequence, heparin-catalyzed inhibition of factor Xa by antithrombin is compromised by fibrinogen t

81 ctivity of the exosite mutant inhibitor with factor Xa by approximately 2-fold but greatly increased

82 tor Va enhances activation of prothrombin by factor Xa by compressing Lnk2 and morphing prothrombin i

83 demonstrated through visualization of bound factor Xa by confocal microscopy using a fluorophore-lab

84 s converted to its catalytically active form factor Xa by the binary complex of factor VIIa bound to

85 Z (PZ), inhibit procoagulant membrane-bound factor Xa by the branched pathway acyl-intermediate trap

86 ically enhance the inhibition of coagulation factor Xa by the serpin, protein Z-dependent protease in

87 w that a specific and selective inhibitor of factor Xa can be engineered by incorporating factor Xa e

88 or, factor VIII, is activated by thrombin or factor Xa-catalyzed cleavage at three P1 residues: Arg-3

89 ngineered stalk with flexible linkers, and a Factor Xa cleavage site was inserted immediately in fron

90 tation of the proteolipid ring in free V(0), factor Xa cleavage sites were introduced between the N-

91 Factor Xa cleaves and activates protease activated recep

92 tion, either alone or in the ternary TF:VIIa:factor Xa coagulation initiation complex.

93 The structure of a factor Xa cocrystal containing 7-fluoroindazole 51a show

94 e effects of dabigatran, the investigational factor Xa decoy andexanet alfa, and the synthetic small

95 (andexanet) is a recombinant modified human factor Xa decoy protein that has been shown to reverse t

96 Antithrombin III and anti-Factor Xa deficiencies and hypercoagulable TEG parameter

97 ally exacerbated by antithrombin III or anti-Factor Xa deficiencies and missed enoxaparin doses.

98 cidence of VTE, bleeding complications, anti-Factor Xa deficiency, and antithrombin III deficiency.

99 sue factor pathway inhibitor (TFPI) produces factor Xa-dependent feedback inhibition of factor VIIa/t

100 to express PAI-1 in response to thrombin and factor Xa did not activate the PAR-1/PAR-2 complex.

101 congeneric ligand pairs for the test system factor Xa, elucidates physical properties of the active-

102 factor Xa can be engineered by incorporating factor Xa exosite and reactive site recognition determin

103 purified reaction mixtures composed only of factor Xa, factor Va, prothrombin, and calcium ions, myo

104 activation and forcing the release of bound factor Xa from the membrane at a venous shear rate (100

105 ibition of Factor VIIa (FVIIa)/tissue factor/Factor Xa (FVIIa/TF/FXa).

106 nformationally pliant variant of coagulation factor Xa (FXa(I16L)) rendered partially inactive by a d

107 Here we found that factor Xa (FXa) activated PAR1 at canonical Arg41 simila

108 doxaban dose, plasma concentration, and anti-Factor Xa (FXa) activity and compared efficacy and safet

109 A number of highly selective and potent factor Xa (FXa) and FIXa inhibitors were identified by s

110 nt (C3b, C5a, C5b-9) in baboons infused with factor Xa (FXa) and phospholipids (FXa/phosphatidylcholi

111 as a cofactor to promote the inactivation of factor Xa (fXa) by PZ-dependent protease inhibitor (ZPI)

112 Protein S (PS) enhances the inhibition of factor Xa (FXa) by tissue factor pathway inhibitor-alpha

113 nt specific inhibitor of membrane-associated factor Xa (fXa) despite having an unfavorable P1 Tyr.

114 PIbeta inhibit both TF-factor VIIa-dependent factor Xa (FXa) generation and free FXa.

115 Factor Xa (FXa) has a prominent role in amplifying both

116 Inhibitors of coagulation factor Xa (fXa) have emerged as a new class of antithrom

117 of the tiger snake, Notechis scutatus, and a factor Xa (FXa) homolog.

118 ivative (6) showing poor thrombin (fIIa) and factor Xa (fXa) inhibition activities, anti-fIIa activit

119 The molecular mechanism of factor Xa (FXa) inhibition by Alboserpin, the major sali

120 approval of fondaparinux, a heparin-derived factor Xa (fXa) inhibitor, provided validation for the d

121 luding direct thrombin inhibitors (DTIs) and factor Xa (FXa) inhibitors, are emerging alternatives fo

122 To test the hypothesis that factor Xa (fXa) interacts with protein S, fXa was labele

123 -soluble phosphatidylserine (C6PS) to bovine factor Xa (FXa) leads to Ca2+-dependent dimerization in

124 Direct inhibitors of coagulation factor Xa (FXa) or thrombin are promising oral anticoagu

125 fied, and assessed for their ability to bind factor Xa (fXa) prior to and following incubation with t

126 Factor Xa (fXa) protects fVa from inactivation by APC.

127 The membrane-dependent interaction of factor Xa (FXa) with factor Va (FVa) forms prothrombinas

128 ombinase is composed of a catalytic subunit, factor Xa (fXa), and a regulatory subunit, factor Va (fV

129 an important anticoagulant role through the factor Xa (FXa)-dependent inhibition of tissue factor/fa

130 d physiological process culminating with the factor Xa (FXa)-mediated conversion of the prothrombin (

131 its tissue factor-factor VIIa (TF-fVIIa) and factor Xa (fXa).

132 converts it to an active cofactor (FVa) for factor Xa (FXa).

133 proved to be potent competitive inhibitor of factor Xa (fXa, Ki = 0.090 nM) and thrombin (fIIa, Ki =

134 ndent protease inhibitor (ZPI) inhibition of factors Xa (FXa) and XIa (FXIa) by a template mechanism.

135 rrower protease specificity, inhibiting only factors Xa (fXa) and XIa.

136 tor-dependent regulator of blood coagulation factors Xa (FXa) and XIa.

137 ctivity at 57 degrees C or in guanidinium by factor Xa generation assays.

138 Parameter values were determined by factor Xa generation assays.

139 reduced decay rates as part of the enzymatic factor Xa generation complex and retained their activiti

140 PDI-accelerated factor Xa generation was blocked by bacitracin but not i

141 In addition, HPC TF initiated factor Xa generation without exogenous factor VIIa, and

142 nd D569A showed >80% reduction in k(cat) for factor Xa generation.

143 Factor Xa has procoagulant activity by conversion of pro

144 romote ZPI inhibition of membrane-associated factor Xa, heparin activates ZPI to inhibit free factor

145 In vitro, ZPI not only inhibits factor Xa in a calcium ion-, phospholipid-, and PZ-depen

146 chieved by tight binding ligands that target factor Xa in a discrete manner.

147 ites of cleavage at Arg(271) and Arg(320) to factor Xa in different orientations by pivoting the C-te

148 has been shown to reverse the inhibition of factor Xa in healthy volunteers.

149 rate constants of antithrombin inhibition of factor Xa in the presence and absence of the designed ac

150 lity to enhance ATIII-mediated inhibition of Factor Xa in vitro.

151 ors, and guanylate cyclase, respectively, in Factor Xa-inhibited (250 nM apixaban), diluted platelet

152 ion of AT activity is approximately 30nM for factor Xa inhibition and 90nM for thrombin inhibition.

153 ti-factor Xa activity, which is a measure of factor Xa inhibition by the anticoagulant.

154 OCKET AF (Rivaroxaban Once-daily oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism

155 In the Rivaroxaban Once Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

156 KET AF (Rivaroxaban Once-daily, oral, direct factor Xa inhibition Compared with vitamin K antagonism

157 KET AF (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

158 In Rivaroxaban Once daily, oral, direct factor Xa inhibition Compared with vitamin K antagonism

159 KET AF (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

160 aroxaban (Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

161 rs in the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

162 trial (Rivaroxaban Once-Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

163 OCKET AF (Rivaroxaban Once-daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism

164 ts in the Rivaroxaban Once Daily Oral Direct Factor Xa Inhibition Compared with Vitamin K Antagonism

165 in the Rivaroxaban Once Daily, Oral, Direct Factor Xa Inhibition Compared With Vitamin K Antagonism

166 d that inhibition of thrombin generation via factor Xa inhibition may further reduce the risk of sten

167 e engineered exosites in alpha1PI to promote factor Xa inhibition.

168 eral anticoagulant that combines an indirect factor Xa inhibitor (fondaparinux analog) and a direct t

169 Apixaban, an oral factor Xa inhibitor administered in fixed doses, may sim

170 xtended-duration thromboprophylaxis with the factor Xa inhibitor betrixaban to reduce the risk of str

171 Whether the oral factor Xa inhibitor edoxaban can be an alternative to wa

172 The oral factor Xa inhibitor edoxaban has demonstrated safety and

173 rombolysis in Myocardial Infarction 48), the factor Xa inhibitor edoxaban was noninferior to warfarin

174 The use of an oral factor Xa inhibitor in patients stabilised after an acut

175 SAR107375), a novel potent dual thrombin and factor Xa inhibitor resulted from a rational optimizatio

176 The factor Xa inhibitor rivaroxaban reduced mortality and is

177 The oral factor Xa inhibitor rivaroxaban was noninferior to warfa

178 s incorporated into a previously established factor Xa inhibitor series.

179 Apixaban, an oral factor Xa inhibitor that can be administered in a simple

180 Rivaroxaban is an oral direct factor Xa inhibitor that has been effective in preventio

181 Apixaban is a novel oral direct factor Xa inhibitor that has been shown to reduce the ri

182 Rivaroxaban is a factor Xa inhibitor that was recently reviewed by the Fo

183 of reproductive age who received direct oral factor Xa inhibitor therapy, of whom 57 had vaginal blee

184 in women of reproductive age on direct oral factor Xa inhibitor therapy.

185 luded because of the intake of a direct oral factor Xa inhibitor which has a strong impact on prothro

186 Edoxaban, an oral factor Xa inhibitor with 50% renal clearance, was noninf

187 erruption, or discontinuation of direct oral factor Xa inhibitor) and the remaining eight (14%) event

188 For each factor Xa inhibitor, a two-part randomized placebo-contr

189 A fixed-dose regimen of rivaroxaban, an oral factor Xa inhibitor, has been shown to be as effective a

190 Apixaban, an oral direct factor Xa inhibitor, is a novel anticoagulant that may r

191 Edoxaban, an oral factor Xa inhibitor, is non-inferior for prevention of s

192 Rivaroxaban, an oral factor Xa inhibitor, may provide more consistent and pre

193 Apixaban, an oral, direct factor Xa inhibitor, may reduce the risk of recurrent is

194 Rivaroxaban, an oral factor Xa inhibitor, might simplify treatment compared w

195 Otamixaban is an intravenous direct factor Xa inhibitor.

196 ithin 18 hours after the administration of a factor Xa inhibitor.

197 he effects of the DTI dabigatran, the direct factor Xa-inhibitor rivaroxaban, and of 2-O, 3-O desulfa

198 Factor Xa inhibitors and aspirin each reduce thrombotic

199 A number of oral direct factor Xa inhibitors and oral direct thrombin inhibitors

200 Compared with warfarin, factor Xa inhibitors are associated with a lower risk of

201 Two direct factor Xa inhibitors are emerging from phase II trials (

202 Oral direct factor Xa inhibitors are potentially well tolerated and

203 Is treatment with factor Xa inhibitors associated with better efficacy and

204 Compared with LMWH, lower doses of oral factor Xa inhibitors can achieve a small absolute risk r

205 Factor Xa inhibitors can prevent 4 instances of symptoma

206 onfatal pulmonary embolism, was reduced with factor Xa inhibitors compared with LMWH (4 fewer events

207 ived data from phase 3 trials of direct oral factor Xa inhibitors done at University Hospital Carl Gu

208 omplications during therapy with direct oral factor Xa inhibitors in a case series of women of reprod

209 ivaroxaban, apixaban, and edoxaban, the oral factor Xa inhibitors in the most advanced stages of deve

210 High, but not lower, doses of oral factor Xa inhibitors increased bleeding compared with LM

211 The direct factor Xa inhibitors may offer several promising alterna

212 in clinical trials suggest that direct oral factor Xa inhibitors might increase menstrual bleeding i

213 Therefore, development of the oral factor Xa inhibitors represents a translational science

214 thrombin inhibitor dabigatran etexilate and factor Xa inhibitors rivaroxaban and apixaban are new or

215 Recently, the oral factor Xa inhibitors rivaroxaban and apixaban have enter

216 loped a novel series of potent and selective factor Xa inhibitors that employ a key 7-fluoroindazolyl

217 In the secondary analysis, factor Xa inhibitors were associated with a reduced risk

218 Factor Xa inhibitors were associated with a reduction in

219 Factor Xa inhibitors were associated with lower rates of

220 se of anticoagulants (vitamin K antagonists, factor Xa inhibitors, and direct thrombin inhibitors) fo

221 s), including direct thrombin inhibitors and factor Xa inhibitors, are emerging options for thrombopr

222 Bleeding is a complication of treatment with factor Xa inhibitors, but there are no specific agents f

223 agulants (nOAC), which includes thrombin and factor Xa inhibitors, has been shown to be effective, bu

224 nhibitor, and rivaroxaban and apixaban, oral factor Xa inhibitors, have been found to be safe and eff

225 oral anticoagulants, such as factor IIa and factor Xa inhibitors, may provide a novel treatment appr

226 twice daily [BID], 110 mg BID), and the oral Factor Xa inhibitors, rivaroxaban and apixaban.

227 inhibitor, dabigatran etexilate, and the two factor Xa inhibitors, rivaroxaban and apixaban.

228 ts with acute major bleeding associated with factor Xa inhibitors, with effective hemostasis occurrin

229 atheter ablation in AF patients treated with factor Xa inhibitors.

230 available in the United States for the oral factor Xa inhibitors.

231 gned to reverse the anticoagulant effects of factor Xa inhibitors.

232 of reproductive age treated with direct oral factor Xa inhibitors: the non-interventional Dresden NOA

233 Various acylcarnitines inhibited factor Xa-initiated clotting.

234 ctively abolishing TF promotes the annexin 2/factor Xa interaction.

235 of the protease domain of human coagulation factor Xa into a bacterial trypsin.

236 lay physiological or pathological roles when factor Xa is generated in a TF-depleted environment.

237 Va(2) (K(d) = approximately 6.5 mum) and to factor Xa (K(d) = approximately 91 mum).

238 ed by 100-fold the apparent Kd of myosin for factor Xa (Kd approximately 0.48 nM), primarily by reduc

239 Cleavage with factor Xa led to further loss of coupling of proton tran

240 Anti-Factor Xa levels in intervention patients were not highe

241 ay require laboratory confirmation with anti-factor Xa levels in patients treated with heparin, espec

242 ion suggest that novel zymogen-like forms of factor Xa might prove useful as new therapeutic procoagu

243 direct oral inhibitor of activated clotting factor Xa, might be more suitable than conventional anti

244 with a preferred IEG substrate sequence for factor Xa modestly enhanced the reactivity of the exosit

245 alyses and native PAGE showed that for every factor Xa molecule inhibited by ZPI, two serpin molecule

246 Here we show that factor Xa mutants with zymogen-like properties (FXa(I16L

247 (Effective aNticaoGulation with factor xA next Generation in Atrial Fibrillation [ENGAGE

248 E AF-TIMI 48 (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation-Thrombo

249 E AF-TIMI 48 (Effective Anticoagulation with factor Xa Next Generation in Atrial Fibrillation-Thrombo

250 IMI 48 trial (Effective Anticoagulation With Factor Xa Next Generation in Atrial Fibrillation-Thrombo

251 E AF-TIMI 48 (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation-Thrombo

252 IMI 48 trial (Effective Anticoagulation with Factor Xa Next Generation in Atrial Fibrillation-Thrombo

253 o regulate the function of blood coagulation factor Xa on membrane surfaces.

254 w here that annexin 2 acts as a receptor for factor Xa on the surface of human umbilical vein endothe

255 uding LMWH, vitamin K antagonists, or direct factor Xa or direct factor IIa inhibitors.

256 First, we found that factor Xa or thrombin activation of PAR-1 led to a rapid

257 f new oral anticoagulants that target either factor Xa or thrombin.

258 vailable anticoagulants that directly target factor Xa or thrombin.

259 oagulants are a class of agents that inhibit factor Xa or thrombin.

260 ated trypsin-like serine proteases thrombin, factor Xa, or activated protein C.

261 ed with low concentrations of tissue factor, factor Xa, or alpha-thrombin.

262 oteolytic activation of FVIII by thrombin or factor Xa, or with its binding to phospholipid surfaces,

263 d the selectivity of alpha1PI for inhibiting factor Xa over thrombin by approximately 1000-fold.

264 In response to thrombotic challenge with factor Xa/phospholipids, EPCR(R84A/R84A) mice generate m

265 Since factor Xa plays a central role in thrombosis, the inhibi

266 complex concentration and thereby attenuate factor Xa production.

267 I were strategically constructed with tandem factor Xa protease cleavage sites in the loop between th

268 rcome this difficulty via the insertion of a Factor Xa proteolytic cleavage site to acquire the optim

269 aelis complex through either ZPI-PZ-lipid or factor Xa-PZ-lipid intermediates was rate-limiting.

270 h independent kinetic analyses of ZPI-PZ and factor Xa-PZ-membrane complex formation suggested that a

271 own for heparin bridging of the antithrombin-factor Xa reaction.

272 lly to accelerate the membrane-dependent ZPI-factor Xa reaction.

273 Maximal accelerations of ZPI-factor Xa reactions required calcium, which augmented th

274 yptophan fluorescence changes and to enhance factor Xa reactivity in antithrombin, indicative of norm

275 ng proteolysis of the factor VIII mutants by factor Xa revealed modest rate reductions (<5-fold) in g

276 at directly inhibit thrombin (dabigatran) or factor Xa (rivaroxaban, apixaban) are effective and safe

277 Direct infusion of factor Xa should also restore hemostasis; however, it ha

278 sion of TF abolishes annexin 2 dependence on factor Xa signaling and diminishes binding to cell surfa

279 rotease activated receptor (PAR)1 or -2, but factor Xa signaling efficiency varies among cell types.

280 We propose that annexin 2 serves to regulate factor Xa signaling specifically in the absence of cell

281 tor Va (KF) and factor Va (AA) had a K D for factor Xa similar to the K D observed for wild-type fact

282 s of the labeled inhibitor with thrombin and factor Xa similar to wild type.

283 tively cleaving the 3-4 loop (via introduced Factor Xa sites) we demonstrate that it plays a vital ro

284 The absence of the Arg173-like residue in factor Xa supported the observed selectivity of inhibiti

285 ing a protease recognition site specific for factor Xa, thrombin, or caspase 3.

286 he MARCKS peptides antagonize the binding of factor Xa to phosphatidylserine and inhibit the enzymati

287 prothrombin is proteolytically converted by factor Xa to the active protease thrombin in a reaction

288 eviously, we found that a novel zymogen-like factor Xa variant (FXa-I16L) was effective in correcting

289 the K(m) for prothrombin conversion with the factor Xa variants assembled into prothrombinase was una

290 8]; warfarin vs dabigatran 0.88 [0.59-1.36]; factor Xa vs low-molecular-weight heparin 1.02 [0.42-2.7

291 th warfarin or low-molecular-weight heparin (factor Xa vs warfarin IRR 0.78 [95% CrI 0.47-1.08]; warf

292 The Gla domain of factor Xa was not required for myosin's prothrombinase e

293 ile the affinity of all mutant molecules for factor Xa was similar to that for factor Va(WT).

294 caspase 3, 1.0nM for thrombin, and 58nM for factor Xa were realized with a scanning fluorometer.

295 , and factor Va(6A) had reduced affinity for factor Xa, when compared to the affinity of the wild-typ

296 PARs) can activate HSCs through thrombin and factor Xa, which are known PAR agonists, and cause micro

297 Mutation of Arg-150 in factor Xa, which interacts with the exosite residues in

298 The interaction of factor Xa with factor Va on membranes to form prothrombi

299 entral role in thrombosis, the inhibition of factor Xa with low-dose rivaroxaban might improve cardio

300 ly results from the binding of RNA(11F7t) to factor Xa with nanomolar affinity in a Ca(2+)-dependent