ライフサイエンスコーパス: antithrombin III

1 ely 914-bp fragment that is 82% identical to antithrombin III.

2 teract directly with the "substrate loop" of antithrombin III.

3 were identified that interact directly with antithrombin III.

4 caused a slight enhancement of inhibition by antithrombin III.

5 ctivation of protein C and the inhibition of antithrombin III.

6 arin's inhibitory effects are independent of antithrombin III.

7 ticoagulant action of heparin is mediated by antithrombin III.

8 ike molecules, which serve as a cofactor for antithrombin III.

9 antiproliferative action is also mediated by antithrombin III.

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

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

12 inhibition by soybean trypsin inhibitor and antithrombin III.

13 ction of factor IXa based on its affinity to antithrombin III.

14 d PAI (less change with transdermal HRT) and antithrombin III.

15 F1+2: 1.539+/-0.03 nmol/L, P<0.001; thrombin-antithrombin III: 1.833+/-0.104 microg/L, P<0.001).

16 groups of 1157 to receive either intravenous antithrombin III (30 000 IU in total over 4 days) or a p

17 ts (18-fold), was resistant to inhibition by antithrombin III (33-fold and 22-fold in the presence an

18 Despite the large size of antithrombin III (58 kDa), no residues outside of the ac

19 Data, including quantification of antithrombin III activity, were collected for these pati

20 It was concluded that antithrombin III, an endogenous inhibitor of thrombin's

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

22 plexes with these inhibitors and cleave both antithrombin III and alpha2-macroglobulin.

23 Antithrombin III and anti-Factor Xa deficiencies and hyp

24 In patients receiving antithrombin III and concomitant heparin, a significantl

25 modifies enzyme/inhibitor functions, such as antithrombin III and heparin cofactor II.

26 EDF based on the X-ray crystal structures of antithrombin III and ovalbumin shows a region at the cen

27 ensive care unit, did not differ between the antithrombin III and placebo groups.

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

29 with significant decreases in the levels of antithrombin III and protein C and an increase in the pl

30 However, 2 potent anticoagulants, antithrombin III and recombinant tissue factor pathway i

31 zyme Xa(TM) hydrolysis is 25%, inhibition by antithrombin III and the tissue factor pathway inhibitor

32 -fold more reactive with Spectrozyme Xa(TM), antithrombin III and tissue factor pathway inhibitor, an

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

34 ules shown previously to dissociate UFH from antithrombin III and to inhibit polyphosphates.

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

36 arin-binding proteins (platelet factor 4 and antithrombin III), and diminished proliferation in some

37 1 of 10 hindered inactivation of thrombin by antithrombin III, and 2 of 10 inhibited inactivation of

38 ibitor, bovine pancreatic trypsin inhibitor, antithrombin III, and alpha2-macroglobulin, whereas acti

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

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

41 of factor V, prothrombin, platelet factor 4, antithrombin III, and fibrinogen.

42 functional activity of protein S, protein C, antithrombin III, and for resistance to activated protei

43 ies to lupus anticoagulant, anticardiolipin, antithrombin III, and the translational product of the f

44 Lys-plasminogen, antithrombin-III, and alteplase were injected through th

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

46 inhibitors tissue factor pathway inhibitor, antithrombin-III, and protein C.

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

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

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

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

51 siologic inhibitors of this pathway TFPI and antithrombin III (AT).

52 nd the minimal length of oligosaccharide for antithrombin III (AT-III) binding.

53 Antithrombin III (AT-III) is an antithrombotic agent wit

54 ide also show an extremely high affinity for antithrombin III (AT-III), a cofactor required for hepar

55 factor VIII, factor V, protein C, protein S, antithrombin III (AT-III), and tissue factor pathway inh

56 important functions is its interaction with antithrombin III (AT-III).

57 ctivity can be traced to its ability to bind antithrombin III (AT-III).

58 tors tissue factor pathway inhibitor (TFPI), antithrombin-III (AT-III) and heparin cofactor-II (HC-II

59 The binding selectivity of antithrombin-III (AT-III) compared well with anti-Factor

60 (TF).VIIa and its product complexes; (b) the antithrombin-III (AT-III)-mediated inactivation of IIa,

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

62 se of the disease in this family could be an antithrombin III (AT3) mutation that resulted in a const

63 Recombinant native antithrombin III (ATIII) and two genetic variants with g

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

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

66 in binding site of the anticoagulant protein antithrombin III (ATIII) has been defined at high resolu

67 Antithrombin III (ATIII) is a key antiproteinase involve

68 equilibrium constant for heparin binding to antithrombin III (ATIII) is a measure of the cofactor's

69 The native conformation of antithrombin III (ATIII) is a poor inhibitor of its coag

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

71 ting heparin where the rate of inhibition by antithrombin III (ATIII) was 15% of normal.

72 eraction with a host of inhibitors including antithrombin III (ATIII), heparin cofactor II (HCII), al

73 human serpins, alpha-1 antitrypsin (AAT) and antithrombin III (ATIII), is described.

74 In vitro binding studies revealed that antithrombin III (ATIII)-thrombin, heparin cofactor II (

75 by the inhibitors C1-inhibitor (C1-INH) and antithrombin III (ATIII).

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

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

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

79 Lys-plasminogen, antithrombin-III (ATIII), and alteplase (tPA) were injec

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

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

82 imilar structural motif to that found in the antithrombin III binding site and having greatly reduced

83 he central and critical residue in heparin's antithrombin III binding site, is responsible for bovine

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

85 pt to prepare oligosaccharides having intact antithrombin III binding sites.

86 ity of this new approach to rapidly assemble antithrombin III-binding classical and non-classical ant

87 We rapidly and efficiently assembled the antithrombin III-binding pentasaccharide in just 6 steps

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

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

90 significantly the clotting time or thrombin-antithrombin III complex (TAT) formation.

91 levels of fibrinogen, D-dimers, and thrombin-antithrombin III complex (TAT) were analyzed.

92 ion as determined by measurement of thrombin-antithrombin III complex formation.

93 09+/-0.119 nmol/L) and formation of thrombin-antithrombin III complexes (125.611+/-6.373 microg/L) wa

94 ted by the plasma concentrations of thrombin-antithrombin III complexes (P < .05).

95 on system (plasma concentrations of thrombin-antithrombin III complexes and prothrombin fragment F1+2

96 , but sodium dodecyl sulfate stable thrombin-antithrombin III complexes are not observed until well a

97 oagulation system (plasma levels of thrombin-antithrombin III complexes) during endotoxemia.

98 oagulation system (plasma levels of thrombin/antithrombin III complexes), nor the activation of the f

99 of prothrombin fragment F1 + 2 and thrombin-antithrombin III complexes).

100 , monitored by the plasma levels of thrombin-antithrombin III complexes, and activation of the fibrin

101 Only sLRP4 bound thrombin-antithrombin III complexes.

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

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

104 in 25 patients who received VenPegC included antithrombin III decrease (52%), elevated transaminases

105 Antithrombin III deficiencies and hypercoagulable TEG pa

106 vious studies have found a high incidence of antithrombin III deficiency among patients with trauma.

107 Patients with an antithrombin III deficiency had fewer mean (SD) ventilat

108 Antithrombin III deficiency was also associated with gre

109 n this cohort study of patients with trauma, antithrombin III deficiency was associated with greater

110 Although antithrombin III deficiency was not significantly associ

111 patients with hypercoagulable states (HCS) (antithrombin III deficiency, protein S or C deficiency,

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

113 ticoagulant activity, as determined using an antithrombin III dependent anti-factor Xa assay.

114 nisms include: first, heparin enhancement of antithrombin III-dependent inhibition of factor V activa

115 onal change observed upon heparin binding to antithrombin III, differences in the affinities of nativ

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

117 T cell receptor beta chain, Ig heavy chain, antithrombin III, Fas ligand, factor V, complement facto

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

119 Experiments carried out in serum (hence antithrombin III)-free medium revealed that heparin's in

120 We demonstrated the specificity of the antithrombin III functionalized sensor for the physiolog

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

122 mortality was nonsignificantly lower in the antithrombin III group (37.8%) than in the placebo group

123 d bleeding incidence was observed (23.8% for antithrombin III group vs 13.5% for placebo group; P<.00

124 ignificant after 90 days (n = 686; 44.9% for antithrombin III group vs 52.5% for placebo group; P =.0

125 Interestingly, this mutant antithrombin III had reduced heparin cofactor activity c

126 The mechanism for heparin activation of antithrombin III has been postulated to involve disrupti

127 of heparin action by APC was independent of antithrombin III, heparin cofactor II, and protein S.

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

129 susceptibility of thrombin to inhibition by antithrombin III in the presence and absence of heparin

130 susceptibility of thrombin to inhibition by antithrombin III in the presence but not in the absence

131 However, the rate of inhibition by antithrombin III in the presence of submaximal concentra

132 e evidence to suggest a treatment benefit of antithrombin III in the subgroup of patients not receivi

133 of the protein C pathway in the presence of antithrombin-III in reactions employing normal factor V

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

135 elatonin prior to anesthesia and intravenous antithrombin III, infliximab, apotransferrin, recombinan

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

137 seropositive individuals modify serum bovine antithrombin III into an HIV-1 inhibitory factor capable

138 Antithrombin III is a plasma protein that functions as a

139 Appropriate timing and dosing of antithrombin III is critical to realize its full therape

140 tcome measurements were associations between antithrombin III levels and outcomes among patients with

141 n associative study, these data suggest that antithrombin III levels may be useful in the risk assess

142 ped a DVT had a more precipitous decrease in antithrombin III levels that were significantly lower th

143 These data indicate that antithrombin III may play a role in the progression of H

144 Antithrombin III may provide protection from multiorgan

145 -145, a peptide derived from the sequence of antithrombin III (n = 9); and pentosan polysulfate (PPS;

146 To this end, the effect of antithrombin III on thrombin-stimulated mesangial cell g

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

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

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

150 isease incidence with factor VII, protein C, antithrombin III, or platelet count.

151 n ischemic stroke incidence and factor VIIc, antithrombin III, platelet count, or activated partial t

152 ation II scores and directly correlated with antithrombin III, protein C, and protein S levels.

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

154 HDL-treated cells bound 40 +/- 5% more 125I-antithrombin III (requires 3-O sulfated HS) and 49 +/- 3

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

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

157 ration was inhibited by standard heparin and antithrombin III, separately or together.

158 nimals showed high-level production of human antithrombin III, similar to the parental transgenic lin

159 n addition, fibrinopeptide A (FPA), thrombin-antithrombin III (TAT) complex formation, and prothrombi

160 he soluble phases were analyzed for thrombin-antithrombin III (TAT) complex formation, prothrombin fr

161 clot times (6.2 to 23 minutes) and thrombin-antithrombin III (TAT) profiles with rates of 25 to 40 n

162 so measured activation of thrombin: thrombin-antithrombin III (TAT), prothrombin fragment 1 + 2 (F1 +

163 us abluminal TNF exposure and was blocked by antithrombin III, TF pathway inhibitor, or anti-TF antib

164 that modulate the inhibition of thrombin by antithrombin III, the principal physiological inhibitor

165 ay be attributable to decreased clearance by antithrombin III, the principal physiological inhibitor

166 High-dose antithrombin III therapy had no effect on 28-day all-cau

167 rboxyl-terminal histidine-tagged recombinant antithrombin III to study the tag on another serpin.

168 e found higher concentrations of antibody to antithrombin III, to a translational product of factor V

169 Overall mortality at 28 days in the antithrombin III treatment group was 38.9% vs 38.7% in t

170 ere obtained to examine its interaction with antithrombin III using microtitration calorimetry.

171 High-dose antithrombin III was associated with an increased risk o

172 The magnitude of the inhibitory action of antithrombin III was equal to that of equimolar concentr

173 PI and factor VLEIDEN was also observed when antithrombin-III was added to the system to complete the

174 onist protamine or the physiological partner antithrombin III were used.

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

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

177 Variant forms of human antithrombin III with glutamine or threonine substitutio

178 amphiphilic 22-residue peptide derived from antithrombin III with seven net charges is only one-twen

179 This decasaccharide bound to antithrombin III with similar avidity as heparin and sho