ライフサイエンスコーパス: antiplasmin

1 d by a neutralizing antibody versus alpha(2)-antiplasmin.

2 NH2-terminal cross-linking domain of alpha2 antiplasmin.

3 li, thrombus dissolution is halted by alpha2-antiplasmin.

4 logical inhibitor, the antiprotease alpha(2)-antiplasmin.

5 dermal fibroblasts in the presence of alpha2-antiplasmin.

6 protect plasmin from inhibition by alpha(2)-antiplasmin.

7 nd derived from the amino terminus of alpha2-antiplasmin.

8 lasmin that is readily inhibited by alpha(2)-antiplasmin.

9 mutants and plasmin were resistant to alpha2-antiplasmin.

10 resistance of the SK-Pm complex to alpha(2)-antiplasmin.

11 protecting plasmin from inhibition by alpha2-antiplasmin.

12 PA, tPA, PAI-1, protease nexin-1, and alpha2-antiplasmin.

13 of wild-type (WT) SK and resistant to alpha2-antiplasmin.

14 ctor, thrombospondin, fibronectin and alpha2-antiplasmin.

15 to inactivation of microplasmin by alpha(2)-antiplasmin.

16 ited the inactivation of plasmin by alpha(2)-antiplasmin.

17 otects plasmin from inactivation by alpha(2)-antiplasmin.

18 tivators, or series inhibition of plasmin by antiplasmins.

19 alpha2-Antiplasmin (A2AP) is a major inhibitor of fibrinolysis

20 hway, including the plasmin inhibitor alpha2-antiplasmin (A2AP).

21 The presence of alpha(2)-antiplasmin abolishes the potentiation of fibrinolysis b

22 smin immunization leads to production of IgG antiplasmin, aCL, and anti-beta(2)GPI in MRL/MpJ mice, b

23 The lack of antiplasmin activity and decreased antitrypsin activity

24 e-dependent effect on coagulation, depleting antiplasmin activity completely, then degrading fibrinog

25 tor to examine the potential role of alpha 2-antiplasmin (alpha 2AP) in experimental pulmonary emboli

26 cross-linking) of plasmin inhibitor alpha(2)-antiplasmin (alpha(2)-AP) into fibrin clots increases th

27 III and the fibrinolytic inhibitor, alpha(2)-antiplasmin (alpha(2)AP) on fibrinolysis.

28 f heart explant cultures with either alpha(2)antiplasmin (alpha(2)AP), a major physiological plasmin

29 vity in clots was measured with (1) alpha(2)-antiplasmin (alpha(2)AP), a physiological glutamine subs

30 The primary inhibitor of plasmin, alpha(2)-antiplasmin (alpha(2)AP), is secreted by the liver into

31 Human alpha(2)-antiplasmin (alpha(2)AP), the main inhibitor of plasmin-

32 amer did react slowly with the serpin alpha2-antiplasmin (alpha2-AP), suggesting a highly limited cat

33 nd inactivating the plasmin inhibitor alpha2-antiplasmin (alpha2-AP).

34 During human blood clotting, alpha2-antiplasmin (alpha2AP) becomes covalently linked to fibr

35 against fibrinolysis by cross-linking alpha2-antiplasmin (alpha2AP) to fibrin.

36 Alpha-2-antiplasmin (alpha2AP) undergoes both N- and C-terminal

37 Human alpha2-antiplasmin (alpha2AP), also known as alpha2-plasmin inh

38 Human alpha2-antiplasmin (alpha2AP, also called alpha2-plasmin inhibi

39 ct the reaction between plasmin and alpha(2)-antiplasmin and accelerate the inactivation of tPA and t

40 In S/D plasma, virtually 100% of the antiplasmin and approximately 50% of the antitrypsin are

41 However, even with complete consumption of antiplasmin and decreases in fibrinogen and factor VIII

42 lasmin is shielded from inhibition by alpha2-antiplasmin and degrades amorphous protein aggregates to

43 PA and plasmin and the eventual depletion of antiplasmin and macroglobulin in an advancing (approxima

44 activator inhibitor-2, antithrombin, alpha 2-antiplasmin and protease nexin I.

45 se-plasmin complex to inhibition by alpha(2)-antiplasmin and was readily inhibited by soybean trypsin

46 sistance of the SK-plasmin complex to alpha2-antiplasmin, and controls fibrin-independent Pg activati

47 , plasminogen activator inhibitors, alpha(2)-antiplasmin, and inflammatory mediators.

48 gulation (DIC) (fibrinogen, D-dimer, alpha-2-antiplasmin, antitrombin, prothrombin time, and platelet

49 Circulating antiplasmin-cleaving enzyme (APCE) has a role in fibrino

50 Circulating antiplasmin-cleaving enzyme (APCE), a prolyl-specific se

51 ng circulation, Met-alpha(2)AP is cleaved by antiplasmin-cleaving enzyme (APCE), yielding Asn-alpha(2

52 a2AP to yield Asn-alpha2AP and have named it antiplasmin-cleaving enzyme (APCE).

53 of alpha2AP is cleaved at the N terminus by antiplasmin-cleaving enzyme (or soluble fibroblast activ

54 o named fibroblast activation protein-alpha, antiplasmin-cleaving enzyme, and dipeptidyl prolyl pepti

55 21% vs 99%, overall P < .01), plasmin-alpha2-antiplasmin complex (520 vs 409 mug/L, overall P = .04),

56 en, t-PA-PAI-1 complex, D-dimer, and plasmin-antiplasmin complex also increased significantly.

57 D-dimer and plasmin-antiplasmin complex levels increased soon after start of

58 , intercellular adhesion molecule-1, plasmin-antiplasmin complex, and D-dimer levels were measured in

59 leukin-6, factor VIIc, factor VIIIc, plasmin-antiplasmin complex, and D-dimer were significantly grea

60 homocysteine, D-dimer, factor VIII, plasmin-antiplasmin complex, and inflammation and coagulation sc

61 tor, platelet activator inhibitor-1, plasmin-antiplasmin complex, D-dimer, thrombin activatable fibri

62 hrombin-antithrombin complex, plasmin-alpha2-antiplasmin complex, plasminogen activator inhibitor typ

63 of coagulation activation), D-dimer, plasmin-antiplasmin complex, tissue plasminogen activator and pl

64 plus thrombin-antithrombin complex, plasmin-antiplasmin complex, tissue plasminogen activator, plasm

65 The concentration of plasmin/antiplasmin complexes (PAP complex) increased by approxi

66 Plasma levels of plasmin-alpha2-antiplasmin complexes increase with the extent of thromb

67 nogen activator activity, and plasmin-alpha2-antiplasmin complexes), followed by inhibition (plasma p

68 ype plasminogen activator and plasmin-alpha2-antiplasmin complexes), whereas TNFR55:IgG did inhibit t

69 ivator inhibitor type I, and plasmin/alpha 2-antiplasmin complexes).

70 tissue plasminogen activator, plasmin-alpha2-antiplasmin complexes, and plasminogen activator inhibit

71 lot or in the circulation by forming plasmin-antiplasmin complexes.

72 ype plasminogen activator and plasmin-alpha2-antiplasmin complexes; P <0.05), but did not influence i

73 and rscuPA, respectively; P < .05), alpha 2-antiplasmin consumption was less (P < .05), and D-dimer

74 ad greater effects than inhibition of alpha2-antiplasmin cross-linking alone (group 4 versus 5; P<0.0

75 ith KA, whereas a plasmin inhibitor, alpha-2-antiplasmin, failed to attenuate KA-induced retinal dama

76 rotect plasmin from inactivation by alpha(2)-antiplasmin, fibrin did protect human plasmin, which for

77 ctor XIIIa-mediated fibrin-fibrin and alpha2-antiplasmin-fibrin cross-linking both caused experimenta

78 ve inhibition of factor XIII-mediated alpha2-antiplasmin-fibrin cross-linking enhanced lysis (group 3

79 iated fibrin-fibrin cross-linking and alpha2-antiplasmin-fibrin cross-linking were measured in anesth

80 TPA (76.0+/-11.9%); and (5) inhibited alpha2-antiplasmin-fibrin cross-linking+TPA (54.7+/-3.9%).

81 use sera were analyzed for production of IgG antiplasmin, IgG aCL, and IgG anti-beta(2)-glycoprotein

82 zed MRL/MpJ mice produced high titers of IgG antiplasmin, IgG aCL, and IgG anti-beta(2)GPI.

83 pJ mice, but leads to production of only IgG antiplasmin in BALB/cJ mice.

84 id A, complement C3, pentraxin 3, and alpha2-antiplasmin in the liver, despite CNS neurodegeneration

85 lasma serpins-antithrombin, antitrypsin, and antiplasmin-in S/D plasma and FFP.

86 a2-antiplasmin levels treated with an alpha2-antiplasmin-inactivating antibody (P<0.0001).

87 linical-dose r-tPA alone (P<0.001) or alpha2-antiplasmin inactivation alone (P<0.001).

88 Dissolution of pulmonary emboli by alpha2-antiplasmin inactivation alone was comparable to 3 mg/kg

89 Despite greater thrombus dissolution, alpha2-antiplasmin inactivation alone, or in combination with l

90 effects of plasminogen activation and alpha2-antiplasmin inactivation on experimental thrombus dissol

91 The effects of r-tPA and alpha2-antiplasmin inactivation on fibrinolysis and bleeding we

92 However, alpha2-antiplasmin inactivation showed a unique pattern of thro

93 olve emboli, but was synergistic with alpha2-antiplasmin inactivation, causing more embolus dissoluti

94 nt with this hypothesis, injection of alpha2-antiplasmin into cerebral ventricles markedly ameliorate

95 kedly accelerated in mice with normal alpha2-antiplasmin levels treated with an alpha2-antiplasmin-in

96 levels, greater than 5-fold elevated plasmin antiplasmin levels, and a complete absence of thrombelas

97 ator of the fibrinolytic system, like alpha2-antiplasmin, may have unique therapeutic value in pulmon

98 Human precursive alpha(2)-antiplasmin (Met-alpha(2)AP), the only known physiologic

99 ntially identical kinetics toward Met-alpha2-antiplasmin (Met-alpha2AP) and peptide substrates.

100 zed BALB/cJ mice produced high titers of IgG antiplasmin only, while plasmin-immunized MRL/MpJ mice p

101 plus the specific plasmin inhibitor alpha(2)-antiplasmin or dermal fibroblasts isolated from plasmino

102 with the adjuvant alone did not develop IgG antiplasmin or IgG aCL.

103 es) and fibrin dissolution (D-dimer; plasmin-antiplasmin or PAP complexes) were also evaluated.

104 as markers of fibrinolysis: plasmin-alpha 2-antiplasmin (PAP) and D-dimer.

105 n-antithrombin [TAT]), fibrinolysis (plasmin-antiplasmin [PAP]), and complement (C3b, C5a, C5b-9) in

106 etic resonance imaging, together with alpha2-antiplasmin peptide (alpha2AP)-targeted perfluorocarbon

107 There were no changes in vWF, and alpha-2-antiplasmin-plasmin complexes increased only in postthro

108 ator inhibitor-1 (PAI-1) Ag and Act, alpha-2-antiplasmin-plasmin complexes, and von Willebrand factor

109 ation process as aprotinin, but not alpha(2)-antiplasmin, prevented collagen dissolution.

110 mine-containing peptides derived from alpha2-antiplasmin, Staphylococcus aureus fibronectin binding p

111 tb-bound plasmin from regulation by alpha(2)-antiplasmin, suggestive of an involvement of this enzyme

112 ained in clots from mice deficient in alpha2-antiplasmin, thrombin-activatable fibrinolysis inhibitor

113 ration of biotinamido-pentylamine and alpha2-antiplasmin to fibrin, and fibrin cross-linking, in cont

114 emboli, assessed the contribution of alpha2-antiplasmin to fibrinolytic failure, and compared the ef

115 Inactivation of alpha2-antiplasmin was comparable to pharmacological r-tPA for

116 Plm inactivation by alpha(2)-antiplasmin was significantly delayed when Plm was prein

117 othrombin fragment 1-2, D-dimer, and plasmin antiplasmin) were measured.