ライフサイエンスコーパス: TAFI

1 TAFI activation, like protein C activation, is augmented

2 TAFI also shares high homology in zinc binding and catal

3 TAFI deficiency did not improve survival rate compared w

4 TAFI is able to reconstitute an APC-dependent shortening

5 TAFI is structurally very similar to pancreatic procarbo

6 TAFI-deficient mice developed normally, reached adulthoo

7 TAFI-deficient mice did not suffer from excess bleeding

8 dP was increased from 50 to 180 minutes in a TAFI concentration-dependent manner.

9 astic strength as controls but also showed a TAFI-dependent delay in fibrinolysis.

10 found to have decreased ability to activate TAFI yet retained normal protein C activation, whereas t

11 s study, we examined the effect of activated TAFI (TAFIa) in modulating the proinflammatory functions

12 e found to be potent inhibitors of activated TAFI and selective versus the related carboxypeptidases

13 talyzed, TM-dependent formation of activated TAFI.

14 Upon activation by thrombin, activated TAFI (TAFIa) attenuates fibrinolysis, presumably by cata

15 body-engineered bispecific inhibitor against TAFI and PAI-1 (heterodimer diabody, Db-TCK26D6x33H1F7)

16 nistration of a bispecific inhibitor against TAFI and PAI-1 results in a prominent profibrinolytic ef

17 rs including PAI-1, alpha 2-antiplasmin, and TAFI were present in samples, which may contribute to th

18 ate its interactions with TM, protein C, and TAFI.

19 rmalized PG, revealing a thrombomodulin- and TAFI-dependent antifibrinolytic mechanism.

20 of HUVECs was abolished 66% by specific anti-TAFI or anti-TM monoclonal antibodies.

21 tribute to the enzymatic differences between TAFI and carboxypeptidase N.

22 tituted purified system, which included both TAFI and either form of factor V purified from pooled pl

23 ivation but was insensitive to inhibition by TAFI.

24 ated by monoclonal antibodies against either TAFI or TM.

25 protein (TBP) and three associated factors (TAFIs), does not have any sequence-specific DNA binding

26 olished thrombomodulin cofactor activity for TAFI activation.

27 Furthermore, TAFI deficiency did not alter kaolin-induced writhing re

28 Intercrossing of heterozygous TAFI mice produced offspring in the expected Mendelian r

29 is inhibitor (TAFI), we generated homozygous TAFI-deficient mice by targeted gene disruption.

30 d thrombomodulin that are required for human TAFI activation.

31 Thus, an impaired TAFI-dependent profibrinolytic response to APC in APC-re

32 Residues important in TAFI activation are located above the active-site cleft,

33 induced hypotension in wild-type, but not in TAFI-deficient, mice in vivo.

34 higher TFPI release and greater reduction in TAFI and fibrinogen levels.

35 MoAbTAFI#16 was shown to inhibit TAFI activation and thereby appears to stimulate fibrino

36 ancing protein C activation while inhibiting TAFI activation, thereby preventing the generation of th

37 thrombin activatable fibrinolysis inhibitor (TAFI) activation.

38 thrombin activatable fibrinolysis inhibitor (TAFI) and fibrinogen were significantly more pronounced

39 thrombin-activatable fibrinolysis inhibitor (TAFI) and plasminogen activator inhibitor-1 (PAI-1) are

40 thrombin-activatable fibrinolysis inhibitor (TAFI) and thereby helps coordinate coagulation, anticoag

41 f thrombin activable fibrinolysis inhibitor (TAFI) in plasma, secondary-extended thrombin generation

42 Thrombin-activable fibrinolysis inhibitor (TAFI) is a recently described plasma zymogen that can be

43 Thrombin-activable fibrinolysis inhibitor (TAFI) is a zymogen that inhibits the amplification of pl

44 e thrombin-activable fibrinolysis inhibitor (TAFI) is activated by thrombin/thrombomodulin on the end

45 Thrombin-activatable fibrinolysis inhibitor (TAFI) is an important regulator of fibrinolysis, and inh

46 Thrombin-activatable fibrinolysis inhibitor (TAFI) is the precursor of an exopeptidase that is identi

47 thrombin-activatable fibrinolysis inhibitor (TAFI) normalized PG, revealing a thrombomodulin- and TAF

48 thrombin activatable fibrinolysis inhibitor (TAFI) production.

49 thrombin-activatable fibrinolysis inhibitor (TAFI), we generated homozygous TAFI-deficient mice by ta

50 thrombin activatable fibrinolysis inhibitor (TAFI).

51 thrombin-activatable fibrinolysis inhibitor (TAFI).

52 thrombin-activatable fibrinolysis inhibitor (TAFI).

53 s thrombin-activable fibrinolysis inhibitor (TAFI).

54 thrombin activatable fibrinolysis inhibitor (TAFI).

55 in the system of purified components lacking TAFI or in plasmas immunodepleted of TAFI.

56 ue autofluorescence/fluorescence imaging (LS-TAFI).

57 ompletely restored when TM/thrombin-mediated TAFI activation was inhibited.

58 , indicating that transmission of the mutant TAFI allele did not lead to embryonic lethality.

59 to activate protein C but maintained normal TAFI activation.

60 In the absence of TAFI, APC did not affect clot lysis in experiments with

61 , PF4 is shown here to inhibit activation of TAFI by thrombin-TM.

62 ed thrombin generation and the activation of TAFI were essentially unopposed by 5A-APC due to its low

63 ion of thrombin and subsequent activation of TAFI, thereby appearing profibrinolytic.

64 Hematological analysis of TAFI-deficient mice did not show any major differences i

65 Through its use, the plasma concentration of TAFI was determined to be 73 nmol/L.

66 The catalytic efficiencies of TAFI and protein C activation by the thrombin-Solulin co

67 human plasma (NHP), plasma immunodepleted of TAFI (TdP), and TdP reconstituted with purified TAFI.

68 lacking TAFI or in plasmas immunodepleted of TAFI.

69 NAc-Hep prevented PF4-mediated inhibition of TAFI activation and the antifibrinolytic functions of TA

70 Consequences of inhibition of TAFI activation by PF4 included loss of TM-dependent pro

71 The kinetics of TAFI and protein C activation by the thrombin-Solulin co

72 e determination of the activatable levels of TAFI in human and other animal plasma in the presence of

73 esidues around the substrate binding site of TAFI resulted in altered C-terminal substrate specificit

74 n an in vitro plasma system, is dependent on TAFI.

75 (EGF)-like domains 1 and 2 had no effect on TAFI or protein C activation, whereas deletions includin

76 To block the inhibitory effects of PF4 on TAFI activation, heparin derivatives were tested for the

77 of both soluble and cellular forms of TM on TAFI activation-dependent suppression of fibrinolysis we

78 effect on thrombin generation, protein C, or TAFI activation could be observed.

79 nfluences lysis time, inhibitors of TAFIa or TAFI activation may prove to be important adjuvants for

80 229K, was able to activate endogenous plasma TAFI in mice, and E229K thrombin infusion effectively bl

81 hrombomodulin EGF-like domain 3 was present, TAFI competitively inhibited protein C activation cataly

82 nimal profibrinolytic activity and preserved TAFI-mediated anti-inflammatory carboxypeptidase activit

83 onal antibody were produced against purified TAFI.

84 nstituted in TdP by the addition of purified TAFI.

85 I (TdP), and TdP reconstituted with purified TAFI.

86 on also revealed that the binding to the TBP-TAFI complex SL1 is not sufficient to activate transcrip

87 ctivation, makes direct contact with the TBP-TAFI complex SL1.

88 the TBP-TAFII complexes, TFIID, and the TBP-TAFI complex, SL1, and in both cases these interactions

89 The current study demonstrates that TAFI deficiency does not change normal responses to acut

90 lin-induced writhing response, implying that TAFI does not play a major role in bradykinin catabolism

91 We expressed wild type TAFI and binding site mutants in 293 cells.

92 In vivo, TAFI deficiency did not influence occlusion time in eith

93 complex requires EGF-like domain 4, whereas TAFI binding also requires EGF-like domain 3.

94 emained to be determined the extent to which TAFI is involved in the profibrinolytic effect of APC in