ライフサイエンスコーパス: antithrombin III

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

2 were identified that interact directly with antithrombin III.

3 caused a slight enhancement of inhibition by antithrombin III.

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

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

6 ticoagulant action of heparin is mediated by antithrombin III.

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

8 antiproliferative action is also mediated by antithrombin III.

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

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

11 inhibition by soybean trypsin inhibitor and antithrombin III.

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

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

14 ely 914-bp fragment that is 82% identical to 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 It was concluded that antithrombin III, an endogenous inhibitor of thrombin's

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

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

22 Antithrombin III and anti-Factor Xa deficiencies and hyp

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

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

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

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

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

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

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

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

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

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

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

34 1 of 10 hindered inactivation of thrombin by antithrombin III, and 2 of 10 inhibited inactivation of

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

61 Antithrombin III (ATIII) is a key antiproteinase involve

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

84 09+/-0.119 nmol/L) and formation of thrombin-antithrombin III complexes (125.611+/-6.373 microg/L) wa

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

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

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

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

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

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

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

92 Only sLRP4 bound thrombin-antithrombin III complexes.

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

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

95 Antithrombin III deficiencies and hypercoagulable TEG pa

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Antithrombin III may provide protection from multiorgan

123 -145, a peptide derived from the sequence of antithrombin III (n = 9); and pentosan polysulfate (PPS;

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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