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1 e activated in vivo by a protease other than factor XIIa.
2 iotensin II, not by neutralizing antibody to factor XIIa.
3 onal serine proteases, MT-SP1/matriptase and Factor XIIa.
4 d the ability to complex with kallikrein and factor XIIa.
5 n was, however, clearly detectable with beta-factor XIIa.
6 icin) without activation, we now report that factor XIIa (0.37 microm), but not factor XII zymogen, i
7 tivity in serum was dependent on coagulation factor XIIa, a serine protease known to induce cleavage
8  nm.min(-1) with thrombin, 6 nm.min(-1) with factor XIIa and 2 nm.min(-1) with factor XIa.
9  group B (binding by a different mechanism), factor XIIa and activated protein C; and group C (no bin
10 ouse studies have demonstrated roles for the factor XIIa and factor XIa in thrombosis.
11 ity levels because inhibition of fluid-phase Factor XIIa and kallikrein requires lower C1INH levels t
12 es of the bradykinin-forming cascade, namely factor XIIa and kallikrein.
13              We showed that serine proteases factor XIIa and plasmin of the coagulation and fibrinoly
14 g, the chimeric proteins were activated with factor XIIa and tested for their capacity to activate fa
15 ective inhibitors of human blood coagulation factor XIIa and thrombin exhibiting a 1,2,4-triazol-5-am
16 stem, murine factor XI is activated by human factor XIIa and thrombin in the presence of dextran sulf
17 inus ticks, which specifically inhibits both factors XIIa and XIa, 2 factors contributing to thrombot
18                                Compared with factors XIIa and XIa, thrombin is the preferred factor X
19 for thrombin, 4.6-50 (mean = 21) min(-1) for factor XIIa, and 1.3-14 (mean = 8) min(-1) for factor XI
20 this position is unable to bind C1r and beta factor XIIa, and also has a decreased rate of reaction w
21 tor of complement C1, plasma kallikrein, and factor XIIa, and as such is involved in regulating infla
22 tituents of the contact pathway: factor XIa, factor XIIa, and plasma kallikrein, in the presence and
23 d platelet aggregation was demonstrated with factor XIIa but not with factor XII zymogen or factor XI
24 s demonstrated experimentally on coagulation factor XIIa by evaluating pairs of fragments with expect
25 as evident regardless of whether we measured factor XIIa-C1-INH or kallikrein-C1-INH complexes, and t
26 r, inactivation of the catalytic activity of factor XIIa did not affect the inhibition of thrombin-in
27 fate as surfaces for factor XI activation by factor XIIa, factor XIa, or thrombin.
28                                              Factor XIIa (FXIIa) and factor XIa (FXIa) contribute to
29  the contact system of coagulation involving factor XIIa (FXIIa) and kallikrein, promoting neutrophil
30                                              Factor XIIa (FXIIa) is a promising target for developing
31  1 (1/2-fXIa) or 2 (fXIa) active subunits by factor XIIa (fXIIa) or thrombin.
32                          FXI is activated by factor XIIa (FXIIa) or thrombin.
33                                Inhibition of factor XIIa (FXIIa) provides thrombus protection without
34 terfere with fXII conversion to the protease factor XIIa (fXIIa).
35 1.38) is the zymogen of the serine protease, factor XIIa (FXIIa).
36 of the proteases plasma kallikrein (PKa) and factor XIIa (FXIIa).
37                                              Factor XIIa had no significant effect on SFLLRN-induced
38            It inhibits mammalian trypsin and Factor XIIa (Hageman Factor) of the contact pathway of c
39 factor XI activation by thrombin (but not by factor XIIa) in the presence of dextran sulfate but not
40 ited with corn trypsin inhibitor (a specific factor XIIa inhibitor without effect on other coagulatio
41 ly convert our ACE-UV method for coagulation factor XIIa into an ACE-MS approach operating at physiol
42  (Ki = 206 nM), factor Xa (Ki = 364 nM), and factor XIIa (Ki = 430 nM).
43 Factor XIII activity showed higher (82%) and factor XIIa lower (38%) heritability.
44 ped using biotinylated activated factor XII (factor XIIa) or biotinylated kallikrein bound to avidin-
45 nternal Arg(369)-Ile(370) bonds by thrombin, factor XIIa, or factor XIa.
46                                   In vivo, a Factor XIIa peritoneal implant generates bypass activity
47 ed kallikrein activity and its generation of factor XIIa, revealing a new pathway for contact system
48                                       Unlike factor XIIa, the ability of rPRCP to activate PK is bloc
49 ctor XI (FXI) including activation of FXI by factor XIIa, thrombin, and autoactivation; and inactivat
50 nted with corn trypsin inhibitor (to inhibit factor XIIa) was perfused over microarrays for 5 minutes
51 asma proteinases, CHFI specifically inhibits Factor XIIa without affecting the activity of other coag
52 n trypsin inhibitor (a specific inhibitor of Factor XIIa without effect on other coagulation factors)