ライフサイエンスコーパス: antithrombin

1 shown potent anti-inflammatory properties of antithrombin.

2 ing in greater protection from inhibition by antithrombin.

3 cing the amount of heparin available to bind antithrombin.

4 mutations causing heparin-binding defects in antithrombin.

5 kisphosphate (TMI) to strongly interact with antithrombin.

6 interact with the heparin binding domain of antithrombin.

7 ive to mFVIIa, but increased inactivation by antithrombin.

8 nts as potential nonsaccharide activators of antithrombin.

9 saturable fluorescence increase, absent with antithrombin.

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

11 action of the pentasaccharide with activated antithrombin.

12 preferentially bind and stabilize activated antithrombin.

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

14 ed during the conversion of native to latent antithrombin.

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

16 those of native rather than those of latent antithrombin.

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

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

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

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

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

22 Antithrombin, a major regulator of coagulation and angio

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

24 th the exosite residues in heparin-activated antithrombin, abrogated the ability of the engineered ex

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

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

27 Only antithrombin activity over time was higher in statin sub

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

29 exadecasaccharide heparin activator enhanced antithrombin affinity for both S195A factor Xa and throm

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

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

35 Antithrombin ameliorates microcirculatory dysfunction an

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

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

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

39 Extracellular serpins such as antithrombin and alpha1-antitrypsin are the quintessenti

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

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

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

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

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

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

46 yl)ethylenediamine (NBD)-fluorophore-labeled antithrombins and accelerated the reactions of the label

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

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

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

50 High-avidity antithrombin antibodies, which prevent antithrombin inac

51 S2'-P2' interaction is involved (factor IX, antithrombin, APPI), beta-branching and increased side c

52 s of plasma serpins alpha(1)-antitrypsin and antithrombin are stable on incubation with the rate-limi

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

54 orm was conformationally altered from native antithrombin as judged from an attenuation of tryptophan

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

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

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

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

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

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

61 Antithrombin (AT) is an anticoagulant serpin that irreve

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

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

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

65 nic activity more potent than that of latent antithrombin, based on the relative abilities of the two

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

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

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

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

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

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

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

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

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

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

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

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

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

79 were assayed for PC, TF, TFPI, and thrombin-antithrombin complex (TATc).

80 e clotting times were shortened and thrombin-antithrombin complex and soluble CD40 ligand levels were

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

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

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

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

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

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

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

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

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

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

94 Markers of thrombin generation (thrombin antithrombin complex, prothrombin fragment 1.2), inflamm

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

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

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

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

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

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

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

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

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

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

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

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

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

110 difference in levels of circulating thrombin-antithrombin complexes.

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

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

113 at the helix D-strand 2A interface of native antithrombin contributes significantly to the stability

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

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

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

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

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

119 Thus, antithrombin deficiency increases the risk of thrombosis

120 Antithrombin deficiency is associated with increased ris

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

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

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

124 Antithrombin deficiency, defined by antithrombin levels

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

126 variant to 9.44 (95% CI, 3.34 to 26.66) for antithrombin deficiency.

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

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

129 ll into 2 classes, based on whether they are antithrombin dependent (low-molecular-weight heparin, fo

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

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

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

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

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

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

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

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

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

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

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

141 t residues Tyr-253 and Glu-255 in the serpin antithrombin function as exosites to promote the inhibit

142 exosites generated by heparin activation of antithrombin function both to promote the formation of a

143 antithrombin deficiency and identified a new antithrombin functional domain.

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

145 Purified prelatent antithrombin had reduced anticoagulant function compared

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

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

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

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

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

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

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

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

154 y thrombin-antithrombin (TAT) production and antithrombin III (ATIII) depletion, Par1(-/-), Par2(-/-)

155 Antithrombin III (ATIII) is a key antiproteinase involve

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

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

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

159 ession of one of these candidate biomarkers, antithrombin III (ATIII).

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

161 Antithrombin III and anti-Factor Xa deficiencies and hyp

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

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

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

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

166 hetic pentasaccharide that mimics the unique Antithrombin III binding domain of heparin possesses wel

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

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

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

170 Antithrombin III deficiencies and hypercoagulable TEG pa

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

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

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

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

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

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

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

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

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

180 1 of 10 hindered inactivation of thrombin by antithrombin III, and 2 of 10 inhibited inactivation of

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

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

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

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

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

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

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

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

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

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

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

192 thrombin released from clots using thrombin-antithrombin immunoassay.

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

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

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

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

197 Antithrombin inactivation of thrombin was impaired in th

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

199 w-molecular-weight heparin, fondaparinux) or antithrombin independent (direct inhibitors of factor Xa

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

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

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

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

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

205 TMI improved antithrombin inhibitory function of plasma from homozygo

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

207 Antithrombin is a key regulator of coagulation and prime

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

209 Kinetic analyses revealed that prelatent antithrombin is an intermediate in the conversion of nat

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

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

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

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

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

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

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

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

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

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

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

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

222 5.90% per patient-year), in 20 patients with antithrombin levels 70% to 80% (5.35% per patient-year),

223 .48; 95% confidence interval, 2.16-5.61) and antithrombin levels 70% to 80% (hazard ratio, 2.40; 95%

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

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

226 Median antithrombin levels were higher while the ETP was lower

227 Thrombin-antithrombin levels were highly correlated with cleaved

228 Mean IgG antithrombin levels were significantly elevated in patie

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

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

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

232 Antithrombin mainly inhibits factor Xa and thrombin.

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

234 and proteolytic susceptibility of prelatent antithrombin most resemble those of native rather than t

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

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

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

238 of heterozygous patients with these specific antithrombin mutations.

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

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

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

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

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

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

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

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

247 Significantly, prelatent antithrombin possessed an antiangiogenic activity more p

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

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

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

251 both to promote the formation of an initial antithrombin-protease Michaelis complex and to favor the

252 in k(on) and decreases in k(off) and caused antithrombin-protease reactions to become diffusion-cont

253 acylation and conformational change steps of antithrombin-protease reactions, we compared the reactio

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

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

256 4.5; P < .001) and highest among carriers of antithrombin, protein C, or protein S deficiency (hazard

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

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

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

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

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

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

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

264 Other antithrombin residues have been suggested to interfere w

265 lized with saline (n = 6); recombinant human antithrombin (rhAT) + heparin, injured and aerosolized w

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

267 ding and kinetic studies with exosite mutant antithrombins showed that Tyr-253 was a critical mediato

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

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

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

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

272 as well as disease activity index, thrombin-antithrombin (TAT) complexes in plasma, and histopatholo

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

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

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

276 lation was activated as measured by thrombin-antithrombin (TAT) production and antithrombin III (ATII

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

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

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

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

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

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

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

284 eases with site-specific fluorophore-labeled antithrombins that allow monitoring of these reaction st

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

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

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

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

289 Equilibrium binding of NBD-labeled antithrombins to S195A proteases showed that exosites ge

290 Heparin activates the serpin, antithrombin, to inhibit its target blood-clotting prote

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

292 Antithrombin variants with altered RCL hinge residues be

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

294 ediate in the conversion of native to latent antithrombin whose formation is favored by stabilizing a

295 tes generated by conformationally activating antithrombin with a heparin pentasaccharide enhanced the

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

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

298 ffects on the reactions of heparin-activated antithrombin with these proteases.

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).