ライフサイエンスコーパス: antithrombin

1 by a stimulatory effect of plasma heparin on antithrombin.

2 shown potent anti-inflammatory properties of antithrombin.

3 ing in greater protection from inhibition by antithrombin.

4 cing the amount of heparin available to bind antithrombin.

5 mutations causing heparin-binding defects in antithrombin.

6 kisphosphate (TMI) to strongly interact with antithrombin.

7 interact with the heparin binding domain of antithrombin.

8 ive to mFVIIa, but increased inactivation by antithrombin.

9 nts as potential nonsaccharide activators of antithrombin.

10 saturable fluorescence increase, absent with antithrombin.

11 ng site and extended heparin-binding site of antithrombin.

12 action of the pentasaccharide with activated antithrombin.

13 preferentially bind and stabilize activated antithrombin.

14 bitor of free factor VIIa in the presence of antithrombin.

15 ed during the conversion of native to latent antithrombin.

16 1)AT), and thrombosis caused by mutations in antithrombin.

17 ide improved prothrombin time, factor X, and antithrombin.

18 tein S, tissue factor pathway inhibitor, and antithrombin.

19 Antithrombin (2.6 muM) plus heparin (4 U/mL) inhibits 72

20 mals was started by intravenous injection of antithrombin (250 IU/kg body weight) or vehicle solution

21 Therapeutic intervention with antithrombin 6 hrs after trauma restored nutritive perfu

22 dings demonstrate that the distal end of the antithrombin A-sheet is crucial for the last steps of pr

23 ivate HCII ca. 250-fold, while leaving aside antithrombin, a closely related serpin, essentially unac

24 Antithrombin, a major regulator of coagulation and angio

25 duce a two-step conformational activation of antithrombin, a process that has remained challenging to

26 nd absence of the designed activators showed antithrombin activation in the range of 8-80-fold in the

27 nd the degree of heparan-sulfate accelerated antithrombin activity on those cells.

28 Only antithrombin activity over time was higher in statin sub

29 d for its functional effects on thrombin and antithrombin activity.

30 Additionally, the antithrombin agent bivalirudin has emerged as a frontrun

31 ional aptamers, it holds promise as a potent antithrombin agent in the treatment of various diseases

32 n (antifactor Xa agents), and dabigatran (an antithrombin agent) were noninferior and probably safer

33 s in patients with type 2 diabetes; a direct antithrombin agent, dabigatran, for reducing stroke and

34 Antiplatelet and direct antithrombin agents may be useful in the prophylaxis of

35 ombin antithrombin (mTAT) and alpha-thrombin antithrombin (alphaTAT) complexes.

36 Antithrombin ameliorates microcirculatory dysfunction an

37 ates and reductions in protein C, protein S, antithrombin and A Disintegrin and Metalloprotease with

38 relatent antithrombin is a mixture of native antithrombin and a modified, true prelatent antithrombin

39 bitors including heparan-sulfate-accelerated antithrombin and activated protein C.

40 Serum levels of antithrombin and anti-activated protein C were compared

41 Thus, complexes between antithrombin and anti-VEGF RNA aptamers with single dith

42 e Lys(114)-independent recognition of native antithrombin and by triggering a Lys(114)-dependent indu

43 bility of heparin to either bridge prelatent antithrombin and coagulation proteases in a ternary comp

44 y of the pentasaccharide to recognize native antithrombin and its ability to preferentially bind and

45 rovides evidence for the interaction between antithrombin and neutrophils in vivo, its pathophysiolog

46 In conclusion, VT after inhibition of antithrombin and protein C is dependent on the presence

47 luating markers of atherothrombosis (fibrin, antithrombin and tissue plasminogen activator [tPA]) and

48 lasminogen activator inhibitor-1, protein C, antithrombin, and endothelial markers (E-selectin, intra

49 ts its activity through direct and indirect (antithrombin- and heparin cofactor II-mediated) inhibiti

50 m APS patients with elevated levels of serum antithrombin antibodies was also tested for its function

51 High-avidity antithrombin antibodies, which prevent antithrombin inac

52 Heparin allosterically activates antithrombin as an inhibitor of factors Xa and IXa by en

53 hibition of factor XIa (fXIa) by the serpins antithrombin (AT) and C1-inhibitor (C1-INH) by more than

54 Antithrombin (AT) and protein Z-dependent protease inhib

55 rence (RNAi) therapeutic (ALN-AT3) targeting antithrombin (AT) as a means to promote hemostasis in he

56 The antithrombin (AT) binding properties of heparin and low

57 The activation of antithrombin (AT) by heparin facilitates the exosite-dep

58 y the serpins heparin cofactor II (HCII) and antithrombin (AT) is accelerated by a heparin template b

59 Antithrombin (AT) is an anticoagulant serpin that irreve

60 Antithrombin (AT) is the most important inhibitor of coa

61 Antithrombin (AT) replacement has been suggested to prev

62 oderately increase the risk, a deficiency in antithrombin (AT), one of the most important natural inh

63 , heparan sulfate, and heparin) and inhibits antithrombin (AT).

64 ere with inactivation of thrombin and FXa by antithrombin (AT).

65 uorometric measurement of affinity displayed antithrombin binding affinities in the low to high micro

66 Overall, the chemo-enzymatic origin and antithrombin binding properties of sulfated DHPs present

67 h have now been found to exhibit interesting antithrombin binding properties.

68 presence of A* residues in both the "normal" antithrombin binding site and also at the nonreducing en

69 oups being both essential and sufficient for antithrombin binding.

70 oxidation/reduction (glycol-split) that lost antithrombin-binding affinity.

71 saccharide residues flanking the "canonical" antithrombin-binding hexasaccharide and the positive pat

72 nging to target with molecules devoid of the antithrombin-binding pentasaccharide DEFGH.

73 ant of heparin pentasaccharide activation of antithrombin both by contributing to the Lys(114)-indepe

74 Heparin is widely used as activator of antithrombin but incurs side effects.

75 the glycosaminoglycan-induced activation of antithrombin by affecting the heparin-binding domain.

76 oglycans allosterically activate the serpin, antithrombin, by binding through a specific pentasacchar

77 Point mutations of antithrombin, C1 inhibitor, alpha(1)-antichymotrypsin, a

78 oresis resolves a limited number of peaks of antithrombin co-complexes suggesting preferential bindin

79 gment 1.2 (F1.2) (1.36-2.4 microM), thrombin-antithrombin complex (14.5-50 microg/L), and D-dimers (6

80 l with dramatic increases in plasma thrombin-antithrombin complex and tissue factor levels.

81 ion with 14E11 suppressed systemic thrombin- antithrombin complex formation, IL-6, and TNF-alpha leve

82 factor production, reducing plasma thrombin-antithrombin complex levels and fibrinogen deposition on

83 seline prothrombin fragment 1.2 and thrombin-antithrombin complex levels in the placebo group; for th

84 ation (bronchoalveolar lavage fluid thrombin-antithrombin complex levels) and PAR-1 immunostaining we

85 ogen activator inhibitor (PAI), and thrombin-antithrombin complex levels, whereas LT and ET only decr

86 nogen activator inhibitor, d-dimer, thrombin antithrombin complex), and lymphocyte cell surface prote

87 ctivation fragment 1+2 (F1+2), TAT (thrombin-antithrombin complex), APC, and D-dimer were monitored o

88 ule-1, E-selectin, P-selectin, TAT (thrombin/antithrombin complex), tumor necrosis factor-alpha, and

89 and -10); "coagulation" (D-dimers, thrombin-antithrombin complex); "oxidative stress" (urine isopros

90 asminogen activator (tPA), d-dimer, thrombin-antithrombin complex, and cytokines (IL-1beta, IL-6, int

91 ased platelet activation, increased thrombin/antithrombin complex, and decreased bleeding times in Cd

92 hibition (prothrombin fragment 1.2, thrombin/antithrombin complex, antithrombin, protein C, activated

93 ndogenous thrombin potential [ETP], thrombin-antithrombin complex, plasmin-alpha2-antiplasmin complex

94 ntional coagulation biomarkers plus thrombin-antithrombin complex, plasmin-antiplasmin complex, tissu

95 hypotension induced E-selectin and thrombin-antithrombin complex, whereas concomitant exposure to bo

96 ound thrombin from inhibition by the heparin-antithrombin complex.

97 aseline prothrombin fragment 1.2 or thrombin-antithrombin complex.

98 seline prothrombin fragment 1.2 and thrombin-antithrombin complex.

99 ncreased local thrombin generation (thrombin antithrombin complex: 8.5 +/- 7.6 ng/ml to 33.2 +/- 17.4

100 sue factor expression, formation of thrombin-antithrombin complexes (p < 0.001), and formation of TNF

101 e of thrombin generation in vitro), thrombin/antithrombin complexes (TAT; a measure of thrombin gener

102 bleeding time and plasma levels of thrombin-antithrombin complexes and tissue factor were measured.

103 eased circulating tissue factor and thrombin-antithrombin complexes in patients with NEC.

104 nchoalveolar lavage fluid levels of thrombin-antithrombin complexes were enhanced in transfusion-rela

105 ed enhanced coagulation activation (thrombin-antithrombin complexes) in plasma.

106 n depletion, and elevated levels of thrombin-antithrombin complexes).

107 Other cytokines, thrombin-antithrombin complexes, and D-dimer were not different b

108 icrovesicle tissue factor activity, thrombin-antithrombin complexes, and D-dimers were measured as pr

109 s evidenced by the increased plasma thrombin-antithrombin complexes, endogenous thrombin potential, a

110 on in the liver and elevated plasma thrombin-antithrombin complexes, indicating activation of coagula

111 stase-alpha1-antitrypsin complexes, thrombin-antithrombin complexes, plasminogen activator activity,

112 postinfection, decreased levels of thrombin-antithrombin complexes, reflecting inhibition of coagula

113 difference in levels of circulating thrombin-antithrombin complexes.

114 cted after endotoxin did not reduce thrombin/antithrombin complexes; nor did antibodies that block AP

115 , patients were randomized to either receive antithrombin concentrate to maintain a plasmatic level 8

116 and 6 hours (p < 0.05, respectively), blood antithrombin concentration was higher at 2 and 4 hours (

117 tifibatide, or abciximab) or anticoagulants (antithrombin dabigatran etexilate or anti-vitamin K acen

118 Repetitive hirudin, a specific potent antithrombin, decreased tumor volume 13- to 24-fold (P <

119 The presence of mild antithrombin deficiency (70-80% antithrombin) in patient

120 thromboplastin time due to cirrhosis-related antithrombin deficiency (heparin cofactor).

121 d I207T, present in individuals with type II antithrombin deficiency and identified a new antithrombi

122 tes that relatives with proteins C and S and antithrombin deficiency are at a significantly higher ri

123 Thus, antithrombin deficiency increases the risk of thrombosis

124 Antithrombin deficiency is associated with increased ris

125 Antithrombin deficiency or the presence of >=1 thromboph

126 inonucleoside model, hyperfibrinogenemia and antithrombin deficiency were also correlated with protei

127 ying patients with protein C, protein S, and antithrombin deficiency who are at increased risk of dev

128 tion of plasma from homozygous patients with antithrombin deficiency with a heparin binding defect an

129 Antithrombin deficiency, defined by antithrombin levels

130 in relatives with protein C, protein S, and antithrombin deficiency, we suggest screening for these

131 FVL and prothrombin G20210A; 9.0% (6.1%) for antithrombin deficiency; 1.1% (0.7%) for protein C defic

132 thrombophilia including proteins C and S and antithrombin deficiency; and Factor (F)V G1691A and FII

133 ility of the active site inhibitor to hinder antithrombin-dependent FXa inactivation, paradoxically a

134 Supplementation of antithrombin did not decrease heparin dose (13.5 interna

135 f each subunit in a polymerization-competent antithrombin dimer.

136 anticoagulant function compared with native antithrombin, due to a reduced heparin affinity and cons

137 RNA interference (RNAi) therapy that targets antithrombin (encoded by SERPINC1), is in development to

138 We measured D-dimers, antithrombin, endogenous thrombin potential (ETP; a func

139 effects of alanine mutations of six putative antithrombin exosite residues and three complementary pr

140 y inhibitor, small interfering RNA to reduce antithrombin expression and the bispecific antibody ACE9

141 interleukin-6, interleukin-10), coagulation (antithrombin, factor IX, plasminogen activator inhibitor

142 previously shown for heparin bridging of the antithrombin-factor Xa reaction.

143 nd anti-coagulant (protein C, protein S, and antithrombin) factors and thrombin generation.

144 rols, including quantified proteins C and S, antithrombin, factors VIII/IX/XI, fibrinogen, lipoprotei

145 nants of UFH effect: UFH dose, age, baseline antithrombin (for anti-Xa), and baseline levels of aPTT

146 antithrombin deficiency and identified a new antithrombin functional domain.

147 We purified alpha- and beta-antithrombin glycoforms from plasma of 2 homozygous L99F

148 Purified prelatent antithrombin had reduced anticoagulant function compared

149 psin), C1 inhibitor, and most efficiently by antithrombin-heparin, but not by elafin, secretory leuko

150 stability and is resistant to inhibition by antithrombin/heparin while still susceptible to small, a

151 nsumption of the natural anticoagulants (low antithrombin, high activated protein C, protein S, and t

152 ons, with fibrin localizing thrombin via its antithrombin-I activity as a potentially self-limiting h

153 the highly specific heparin-binding protein antithrombin III (AT III).

154 In this work we used heat-stressed human antithrombin III (AT), a 58 kDa glycoprotein, to compare

155 l enzyme involved in the biosynthesis of the antithrombin III (AT)-binding site in the biopharmaceuti

156 es, we show that disruption of the zebrafish antithrombin III (at3) locus results in spontaneous veno

157 ous biochemical assays, and the human serpin antithrombin III (ATIII) as a model, we explored the rol

158 Antithrombin III (ATIII) is a key antiproteinase involve

159 The serpin antithrombin III (ATIII) targets thrombin and other prot

160 ll as low molecular weight heparin-activated antithrombin III (ATIII).

161 ry of heparin hexasaccharides for binders to antithrombin III (ATIII).

162 ion analysis of a blood coagulation protein, antithrombin III and a protease, cathepsin D, showcases

163 Antithrombin III and anti-Factor Xa deficiencies and hyp

164 es the binding specificity of HS/heparin for antithrombin III and plays a key role in herpes simplex

165 ligands and are resistant to inactivation by antithrombin III and tissue factor pathway inhibitor.

166 increased affinity for fluorescently labeled antithrombin III as detected by confocal microscopy.

167 Clinically, recombinant human antithrombin III attenuated the increased pulmonary tran

168 -sulfo groups in BIH increases the number of antithrombin III binding sites, making remodeled BIH beh

169 actor by 22% (95% CI, -35% to -9%), thrombin-antithrombin III by 16% (95% CI, -19% to -13%), high-sen

170 I, and von Willebrand factor and decrease in antithrombin III correlated with metabolic features, but

171 Antithrombin III deficiencies and hypercoagulable TEG pa

172 omplications, anti-Factor Xa deficiency, and antithrombin III deficiency.

173 asaccharide motif known to interact with the antithrombin III domain and act as anticoagulant.

174 ribe the creation of a null mutation for the antithrombin III gene (at3) in zebrafish by using zinc f

175 e therapeutic potential of recombinant human antithrombin III in a large animal model of acute lung i

176 ty and mortality, potentially exacerbated by antithrombin III or anti-Factor Xa deficiencies and miss

177 IV infusion of 6 IU/kg/hr recombinant human antithrombin III or normal saline (n = 6 each) during th

178 lable states, caused by deficiency of either antithrombin III or protein C.

179 mpared to control animals, recombinant human antithrombin III reduced the number of neutrophils per h

180 Treatment with recombinant human antithrombin III resulted in a reduction of pulmonary ni

181 (prothrombin fragment 1+2) and TAT (thrombin-antithrombin III) were assessed immediately before the p

182 is (D-dimer, von Willebrand factor, thrombin-antithrombin III), inflammation (high-sensitivity C-reac

183 1 of 10 hindered inactivation of thrombin by antithrombin III, and 2 of 10 inhibited inactivation of

184 r C1-INH protein, C1q, alpha2-macroglobulin, antithrombin III, and angiotensin-converting enzyme.

185 (sCD40L, plasminogen activator inhibitor 1, antithrombin III, and C-reactive protein).

186 ogen-like character, including resistance to antithrombin III, correlates well with plasma half-life

187 time <= 50 s, international normalized ratio antithrombin III, fibrinogen, plasma-free hemoglobin, pl

188 s of therapy were TSP4, TIMP-2, SEPR, MRC-2, Antithrombin III, SAA, CRP, NPS-PLA2, LEAP-1, and LBP.

189 rotein-3 and acid-labile subunit, along with antithrombin III, were all deficient in Pmm2(R137H/F115L

190 tetrasaccharides are derived from heparin's antithrombin III-binding sites, we examined whether this

191 higher BMIs for all measurements, except for antithrombin III.

192 and 2 of 10 inhibited inactivation of FXa by antithrombin III.

193 (d-dimer), and lower coagulation biomarkers (antithrombin-III and factor IX) (p < 0.05).

194 tumor necrosis factor, IL-6, IL-10, d-dimer, antithrombin-III, and factor IX (adjusted HR = 1.27, p =

195 formed by intact unfractionated heparin and antithrombin-III, interaction which is central to preven

196 thrombin released from clots using thrombin-antithrombin immunoassay.

197 s of the coagulation markers DD and thrombin antithrombin in pathogenic SIV infections of rhesus and

198 used by pathogenic polymerization of mutated antithrombin in the blood.

199 ence of mild antithrombin deficiency (70-80% antithrombin) in patients with unprovoked VTE is associa

200 ity for thrombin and significantly inhibited antithrombin inactivation of thrombin compared with IgG

201 Antithrombin inactivation of thrombin was impaired in th

202 idity antithrombin antibodies, which prevent antithrombin inactivation of thrombin, distinguish patie

203 G) is a fucosylated chondroitin sulfate with antithrombin-independent antithrombotic properties.

204 anges and to enhance factor Xa reactivity in antithrombin, indicative of normal conformational activa

205 Allosteric conformational changes in antithrombin induced by binding a specific heparin penta

206 IIa, and displayed similar FX activation and antithrombin inhibition kinetics to the FVIIa.sTF comple

207 easurement of second-order rate constants of antithrombin inhibition of factor Xa in the presence and

208 for p-aminobenzamidine, an increased rate of antithrombin inhibition, an increased rate of incorporat

209 TMI improved antithrombin inhibitory function of plasma from homozygo

210 tor Xa as they do with the heparin-activated antithrombin interaction.

211 Antithrombin is a key regulator of coagulation and prime

212 that the previously characterized prelatent antithrombin is a mixture of native antithrombin and a m

213 heparin-catalyzed inhibition of factor Xa by antithrombin is compromised by fibrinogen to a greater e

214 eric activation of the anticoagulant serpin, antithrombin, is the release of the reactive center loop

215 However, exogenous antithrombin itself may increase the risk of bleeding.

216 n resulted in dose-dependent lowering of the antithrombin level and increased thrombin generation in

217 A reduction in the antithrombin level of more than 75% from baseline result

218 therapy exposure was associated with a lower antithrombin level, a lower nAPCsr, and a lower ETP, whi

219 on, as measured by the ETP, and an increased antithrombin level.

220 per patient-year), and in 214 patients with antithrombin levels >80% (3.31% per patient-year).

221 rval, 1.51-3.80) compared with patients with antithrombin levels >80%.

222 VTE recurrence occurred in 19 patients with antithrombin levels <70% (5.90% per patient-year), in 20

223 ce was significantly higher in patients with antithrombin levels <70% (hazard ratio, 3.48; 95% confid

224 VTE were stratified according to functional antithrombin levels (<70%, 70-80%, >80%) and were follow

225 current VTE associated with mildly decreased antithrombin levels (70-80%).

226 1), activated clotting time (p = 0.001), and antithrombin levels (p = 0.02), but not with internation

227 5.90% per patient-year), in 20 patients with antithrombin levels 70% to 80% (5.35% per patient-year),

228 .48; 95% confidence interval, 2.16-5.61) and antithrombin levels 70% to 80% (hazard ratio, 2.40; 95%

229 tion with hepatic steatosis, plasma thrombin-antithrombin levels and hepatic fibrin deposition increa

230 Antithrombin deficiency, defined by antithrombin levels of <70%, is a major thrombophilic co

231 Median antithrombin levels were higher while the ETP was lower

232 Thrombin-antithrombin levels were highly correlated with cleaved

233 Mean IgG antithrombin levels were significantly elevated in patie

234 in wild-type mice increased tPA and thrombin-antithrombin levels, and the latter was reversed by L-me

235 With stratification for antithrombin levels, VTE recurrence occurred in 19 patie

236 he coagulation system, with the exception of antithrombin levels, which were less decreased in calciu

237 Antithrombin mainly inhibits factor Xa and thrombin.

238 peculated that the natural beta-glycoform of antithrombin might compensate for the effect of heparin-

239 Supplementation of antithrombin might decrease the amount of heparin needed

240 ere developed that measure the meizothrombin antithrombin (mTAT) and alpha-thrombin antithrombin (alp

241 mbinant R47C and P41L, other heparin-binding antithrombin mutants.

242 owever, patients homozygous for L99F or R47C antithrombin mutations are viable.

243 of heterozygous patients with these specific antithrombin mutations.

244 polymer formation, and helix D is a site (in antithrombin) of allosteric regulation.

245 We herein report on the action of antithrombin on skeletal muscle injury in experimental e

246 ed were the nuclear protein-coding genes for antithrombin or SerpinC, Immunoglobulin lambda light cha

247 on regimens, including heparin, heparinoids, antithrombins, or fibrinolytics (e.g., tissue plasminoge

248 this role, we expressed and characterized 15 antithrombin P14 variants.

249 oximately 60% loss in binding energy for the antithrombin-pentasaccharide interaction due to the disr

250 he Lys(114) binding partner of this group on antithrombin-pentasaccharide interactions by equilibrium

251 uture development of pharmaceuticals against antithrombin polymerization, an improved understanding o

252 ta-hairpin runaway domain swap mechanism for antithrombin polymerization.

253 tary sources of conformational activation of antithrombin, probably involving altered contacts of sid

254 e with RCL insertion or the stability of the antithrombin-protease complex, but available crystal str

255 e final docking site for the protease in the antithrombin-protease complex, supporting the idea that

256 fragment 1.2, thrombin/antithrombin complex, antithrombin, protein C, activated protein C, protein S,

257 iciencies of the natural anticoagulants (ie, antithrombin, protein C, and protein S), were assessed,

258 4.5; P < .001) and highest among carriers of antithrombin, protein C, or protein S deficiency (hazard

259 among family members found to be carriers of antithrombin, protein C, or protein S deficiency, 0.42%

260 atives of 206 pediatric VTE patients for IT (antithrombin, protein C, protein S, factor V G1691A, fac

261 rtance of all residues for heparin-activated antithrombin reactivity and Arg(150) for native serpin r

262 ate that the exosite is a key determinant of antithrombin reactivity with factors Xa and IXa in the n

263 e complementary protease exosite residues on antithrombin reactivity with these proteases in unactiva

264 egimen induced a dose-dependent mean maximum antithrombin reduction of 70 to 89% from baseline.

265 e randomized to the open-label use of 1 of 3 antithrombin regimens (heparin plus a glycoprotein IIb/I

266 Other antithrombin residues have been suggested to interfere w

267 ned inhibition of the natural anticoagulants antithrombin (Serpinc1) and protein C (Proc) using small

268 Mice deficient in the anticoagulants antithrombin (Serpinc1) or protein C (Proc) display prem

269 dence of binding affinity indicates that the antithrombin-sulfated DHP interaction involves a massive

270 conceived a study to evaluate the effect of antithrombin supplementation in adult patients requiring

271 Antithrombin supplementation may not decrease heparin re

272 When applied to a paradigmatic heparin/antithrombin system, the new method generates a series o

273 d the measured clot elution rate of thrombin-antithrombin (TAT) and fragment F1.2 in the presence and

274 ast 99% for 10 days, and suppressed thrombin-antithrombin (TAT) complex and beta-thromboglobulin (bet

275 plasma contained markedly elevated thrombin-antithrombin (TAT) complex levels (indicating uncontroll

276 asurement of C-peptide, proinsulin, thrombin-antithrombin (TAT) complex, and a panel of proinflammato

277 , indicated by the concentration of thrombin-antithrombin (TAT) complexes in plasma.

278 After injury, circulating thrombin-antithrombin (TAT) complexes were lower after short vers

279 nhematopoietic cells reduced plasma thrombin-antithrombin (TAT) levels 8 hours after administration o

280 Thrombin generation (thrombin-antithrombin [TAT] complex), endothelial dysfunction (as

281 tivation biomarkers of coagulation (thrombin-antithrombin [TAT]), fibrinolysis (plasmin-antiplasmin [

282 antithrombin and a modified, true prelatent antithrombin that are resolvable by heparin-agarose chro

283 led that TMI induced a partial activation of antithrombin that facilitated the interaction with hepar

284 ndent induced fit interaction with activated antithrombin that locks the serpin in the activated stat

285 e that limited conformational alterations of antithrombin that modestly reduce anticoagulant activity

286 A conformationally altered prelatent form of antithrombin that possesses both anticoagulant and antia

287 imizing adjunct pharmacology including early antithrombin therapy preloading with a potent antiplatel

288 These findings suggest that in WT antithrombin there are two major complementary sources o

289 a synthetic pentasaccharide, which binds to antithrombin, thereby indirectly inhibiting factor Xa.

290 We tested the efficacy of antiplatelet and antithrombin to prevent experimental IE.

291 Mutations of antithrombin Tyr(253) and His(319) exosite residues prod

292 Antithrombin variants with altered RCL hinge residues be

293 Antithrombin was 109.5% (93.0-123.0%) in the treatment g

294 captured by intrathrombus fibrin as thrombin-antithrombin was largely undetectable in the effluent un

295 as higher, whereas protein C, protein S, and antithrombin were all lower, which, together with increa

296 Enhanced 3-O-sulfation increased binding to antithrombin, which enhanced Factor Xa inhibition, and b

297 EP217609 bound antithrombin with high affinity (K(D) = 30nM) and activa

298 studies indicate that sulfated DHPs bind to antithrombin with micromolar affinity under physiologica

299 enous fluorescence indistinguishable from WT antithrombin yet, in the absence of heparin, shows massi

300 promoting mutations in the 131-136 region of antithrombin (YRKAQK to LEEAAE).