ライフサイエンスコーパス: ATIII

1 ATIII has three disulfide bonds, two near the N terminus

2 ATIII RNA transcripts were identified within CNS lymphom

3 ATIII, HCII, and alpha2-M are all abundant in blood and

4 proteases involved in blood coagulation, and ATIII misfolding can thus lead to thrombosis and other d

5 nteractions to promote P-helix formation and ATIII binding to the pentasaccharide.

6 0(3) and 0.91 x 10(3) M-1 s-1 for C1-INH and ATIII, respectively.

7 ts were identified within CNS lymphomas, and ATIII protein was localized selectively to tumor neovasc

8 inability of a number of disease-associated ATIII variants to navigate the folding reaction helps to

9 which resembles the naturally occurring beta-ATIII isoform in its interactions with high affinity hep

10 and (1:2:3:9:0), only two are shown to bind ATIII, namely, (1:2:3:8:0) and (1:2:3:9:0).

11 e specificity of the hexasaccharides binding ATIII was confirmed by assaying their ability to enhance

12 Inhibition of FXIa by ATIII in the presence of heparin was decreased 4-fold by

13 ns (0.1-1.0 units/ml) enhanced inhibition by ATIII 20-55-fold compared with 0.1-7.0-fold for C1-INH.

14 st bind to heparin for optimal inhibition by ATIII and for autoactivation.

15 ative, heparin-bound, complexed, and cleaved ATIII molecules for heparin can be explained based on th

16 Measurement of CSF ATIII levels was found to potentially enhance the abilit

17 antibacterial effects of intact and degraded ATIII.

18 nfirmed by assaying their ability to enhance ATIII-mediated inhibition of Factor Xa in vitro.

19 ogether, our results suggest novel roles for ATIII-derived peptide fragments in host defense.

20 ed that Tyr(131) might serve as a switch for ATIII conformational activation.

21 ected increases in blood loss resulting from ATIII-dependent anticoagulation by enoxaparin or fondapa

22 fficient folding and secretion of functional ATIII.

23 ptide FFFAKLNCRLYRKANKSSKLV (FFF21) of human ATIII, was found to be antimicrobial against particularl

24 Recombinant native antithrombin III (ATIII) and two genetic variants with glutamine substitut

25 ombin (TAT) production and antithrombin III (ATIII) depletion, Par1(-/-), Par2(-/-), Par4(-/-), Par2(

26 the anticoagulant protein antithrombin III (ATIII) has been defined at high resolution by alanine sc

27 Antithrombin III (ATIII) is a key antiproteinase involved in blood coagula

28 ant for heparin binding to antithrombin III (ATIII) is a measure of the cofactor's binding to and act

29 The native conformation of antithrombin III (ATIII) is a poor inhibitor of its coagulation pathway ta

30 The serpin antithrombin III (ATIII) targets thrombin and other proteases involved in

31 the rate of inhibition by antithrombin III (ATIII) was 15% of normal.

32 st of inhibitors including antithrombin III (ATIII), heparin cofactor II (HCII), alpha2-macroglobulin

33 ding studies revealed that antithrombin III (ATIII)-thrombin, heparin cofactor II (HCII)-thrombin, an

34 r weight heparin-activated antithrombin III (ATIII).

35 saccharides for binders to antithrombin III (ATIII).

36 hese candidate biomarkers, antithrombin III (ATIII).

37 C1-inhibitor (C1-INH) and antithrombin III (ATIII).

38 aracterization of the biologically important ATIII binding pentasaccharide and its precursors, which

39 e positions in the structure of P14-inserted ATIII and models of native antithrombin, derived from th

40 In contrast to intact ATIII, the results showed that extensive degradation of

41 w that the Tyr(131) ring is buried in native ATIII and then becomes exposed when pentasaccharide bind

42 Recombinant native ATIII and all of the variants had very similar second or

43 lded a Kd of 6 nM for the recombinant native ATIII and K136T, whereas K114Q and K139Q bound heparin s

44 Recombinant native ATIII was nearly identical to plasma-purified ATIII, whe

45 rly identical to those of recombinant native ATIII, indicating that the glutamine substitutions did n

46 that required to activate recombinant native ATIII.

47 r switch during the allosteric activation of ATIII anticoagulant activity.

48 predominant factor in heparin activation of ATIII thrombin inhibition, and removal of the P1 constra

49 n the pentasaccharide-mediated activation of ATIII toward factor Xa.

50 as found to be critical in the activation of ATIII toward factor Xa.

51 n the pentasaccharide-mediated activation of ATIII.

52 n the pentasaccharide-mediated activation of ATIII.

53 nstrated that RAP inhibited the clearance of ATIII-125I-thrombin complexes from the circulation.

54 Determination of ATIII concentration by ELISA was significantly more accu

55 Our studies of ATIII in-cell folding reveal a surprising, biased order

56 , line a 50-A long channel on the surface of ATIII.

57 tithrombin which is highly similar to plasma ATIII in its inhibition of thrombin and factor Xa and wh

58 TIII was nearly identical to plasma-purified ATIII, whereas K114Q and K139Q were severely impaired in

59 to 125I-thrombin in complex with the serpins ATIII, HCII, alpha1-proteinase inhibitor, or d-phenylala

60 arly folding of the predominantly beta-sheet ATIII domain in this two-domain protein constrains the r

61 Previous investigations have shown that ATIII is degraded by Staphylococcus aureus V8 protease,

62 e helix D-sheet A interface, adjacent to the ATIII pentasaccharide and heparin cofactor-binding sites

63 s in the high affinity binding of heparin to ATIII and the activation of thrombin inhibitory activity

64 E255A and wild-type ATIIIs have identical reactive loop sequences (including