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1                                              ATIII has three disulfide bonds, two near the N terminus
2                                              ATIII RNA transcripts were identified within CNS lymphom
3                                              ATIII variants with free thiols were retained in the end
4                                              ATIII, HCII, and alpha2-M are all abundant in blood and
5                                     Although ATIII has N-glycans and a hydrophobic core, we found tha
6 proteases involved in blood coagulation, and ATIII misfolding can thus lead to thrombosis and other d
7 nteractions to promote P-helix formation and ATIII binding to the pentasaccharide.
8 0(3) and 0.91 x 10(3) M-1 s-1 for C1-INH and ATIII, respectively.
9 ts were identified within CNS lymphomas, and ATIII protein was localized selectively to tumor neovasc
10  inability of a number of disease-associated ATIII variants to navigate the folding reaction helps to
11 which resembles the naturally occurring beta-ATIII isoform in its interactions with high affinity hep
12  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).
13 e specificity of the hexasaccharides binding ATIII was confirmed by assaying their ability to enhance
14                        Inhibition of FXIa by ATIII in the presence of heparin was decreased 4-fold by
15 ns (0.1-1.0 units/ml) enhanced inhibition by ATIII 20-55-fold compared with 0.1-7.0-fold for C1-INH.
16 st bind to heparin for optimal inhibition by ATIII and for autoactivation.
17 ative, heparin-bound, complexed, and cleaved ATIII molecules for heparin can be explained based on th
18                                 In contrast, ATIII, which has more C-terminal glycans, is initially h
19                           Measurement of CSF ATIII levels was found to potentially enhance the abilit
20 antibacterial effects of intact and degraded ATIII.
21 nfirmed by assaying their ability to enhance ATIII-mediated inhibition of Factor Xa in vitro.
22 ogether, our results suggest novel roles for ATIII-derived peptide fragments in host defense.
23 ed that Tyr(131) might serve as a switch for ATIII conformational activation.
24 ected increases in blood loss resulting from ATIII-dependent anticoagulation by enoxaparin or fondapa
25 fficient folding and secretion of functional ATIII.
26 ptide FFFAKLNCRLYRKANKSSKLV (FFF21) of human ATIII, was found to be antimicrobial against particularl
27         Recombinant native antithrombin III (ATIII) and two genetic variants with glutamine substitut
28 says, and the human serpin antithrombin III (ATIII) as a model, we explored the role of ERQC systems
29 ombin (TAT) production and antithrombin III (ATIII) depletion, Par1(-/-), Par2(-/-), Par4(-/-), Par2(
30  the anticoagulant protein antithrombin III (ATIII) has been defined at high resolution by alanine sc
31                            Antithrombin III (ATIII) is a key antiproteinase involved in blood coagula
32 ant for heparin binding to antithrombin III (ATIII) is a measure of the cofactor's binding to and act
33 The native conformation of antithrombin III (ATIII) is a poor inhibitor of its coagulation pathway ta
34                 The serpin antithrombin III (ATIII) targets thrombin and other proteases involved in
35  the rate of inhibition by antithrombin III (ATIII) was 15% of normal.
36 st of inhibitors including antithrombin III (ATIII), heparin cofactor II (HCII), alpha2-macroglobulin
37 ha-1 antitrypsin (AAT) and antithrombin III (ATIII), is described.
38 ding studies revealed that antithrombin III (ATIII)-thrombin, heparin cofactor II (HCII)-thrombin, an
39 r weight heparin-activated antithrombin III (ATIII).
40 saccharides for binders to antithrombin III (ATIII).
41 hese candidate biomarkers, antithrombin III (ATIII).
42  C1-inhibitor (C1-INH) and antithrombin III (ATIII).
43           Lys-plasminogen, antithrombin-III (ATIII), and alteplase (tPA) were injected through the re
44 aracterization of the biologically important ATIII binding pentasaccharide and its precursors, which
45       Mutagenesis of all six Cys residues in ATIII to Ala resulted in its efficient secretion even th
46 e positions in the structure of P14-inserted ATIII and models of native antithrombin, derived from th
47                        In contrast to intact ATIII, the results showed that extensive degradation of
48 w that the Tyr(131) ring is buried in native ATIII and then becomes exposed when pentasaccharide bind
49                           Recombinant native ATIII and all of the variants had very similar second or
50 lded a Kd of 6 nM for the recombinant native ATIII and K136T, whereas K114Q and K139Q bound heparin s
51                           Recombinant native ATIII was nearly identical to plasma-purified ATIII, whe
52 rly identical to those of recombinant native ATIII, indicating that the glutamine substitutions did n
53 that required to activate recombinant native ATIII.
54 r switch during the allosteric activation of ATIII anticoagulant activity.
55  predominant factor in heparin activation of ATIII thrombin inhibition, and removal of the P1 constra
56 n the pentasaccharide-mediated activation of ATIII toward factor Xa.
57 as found to be critical in the activation of ATIII toward factor Xa.
58 n the pentasaccharide-mediated activation of ATIII.
59 n the pentasaccharide-mediated activation of ATIII.
60 nstrated that RAP inhibited the clearance of ATIII-125I-thrombin complexes from the circulation.
61                             Determination of ATIII concentration by ELISA was significantly more accu
62                               Our studies of ATIII in-cell folding reveal a surprising, biased order
63 , line a 50-A long channel on the surface of ATIII.
64 tithrombin which is highly similar to plasma ATIII in its inhibition of thrombin and factor Xa and wh
65 TIII was nearly identical to plasma-purified ATIII, whereas K114Q and K139Q were severely impaired in
66 to 125I-thrombin in complex with the serpins ATIII, HCII, alpha1-proteinase inhibitor, or d-phenylala
67 arly folding of the predominantly beta-sheet ATIII domain in this two-domain protein constrains the r
68      Previous investigations have shown that ATIII is degraded by Staphylococcus aureus V8 protease,
69 e helix D-sheet A interface, adjacent to the ATIII pentasaccharide and heparin cofactor-binding sites
70 s in the high affinity binding of heparin to ATIII and the activation of thrombin inhibitory activity
71                          E255A and wild-type ATIIIs have identical reactive loop sequences (including