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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 
  
     9  group B (binding by a different mechanism), factor XIIa and activated protein C; and group C (no bin
  
    11 ity levels because inhibition of fluid-phase Factor XIIa and kallikrein requires lower C1INH levels t
  
  
    14 g, the chimeric proteins were activated with factor XIIa and tested for their capacity to activate fa
    15 stem, murine factor XI is activated by human factor XIIa and thrombin in the presence of dextran sulf
  
    17 for thrombin, 4.6-50 (mean = 21) min(-1) for factor XIIa, and 1.3-14 (mean = 8) min(-1) for factor XI
    18 this position is unable to bind C1r and beta factor XIIa, and also has a decreased rate of reaction w
    19 tor of complement C1, plasma kallikrein, and factor XIIa, and as such is involved in regulating infla
    20 tituents of the contact pathway: factor XIa, factor XIIa, and plasma kallikrein, in the presence and 
    21 d platelet aggregation was demonstrated with factor XIIa but not with factor XII zymogen or factor XI
    22 as evident regardless of whether we measured factor XIIa-C1-INH or kallikrein-C1-INH complexes, and t
    23 r, inactivation of the catalytic activity of factor XIIa did not affect the inhibition of thrombin-in
  
  
  
  
  
  
  
  
    32 factor XI activation by thrombin (but not by factor XIIa) in the presence of dextran sulfate but not 
    33 ited with corn trypsin inhibitor (a specific factor XIIa inhibitor without effect on other coagulatio
  
  
    36 ped using biotinylated activated factor XII (factor XIIa) or biotinylated kallikrein bound to avidin-
  
  
    39 ed kallikrein activity and its generation of factor XIIa, revealing a new pathway for contact system 
  
    41 ctor XI (FXI) including activation of FXI by factor XIIa, thrombin, and autoactivation; and inactivat
    42 nted with corn trypsin inhibitor (to inhibit factor XIIa) was perfused over microarrays for 5 minutes
    43 asma proteinases, CHFI specifically inhibits Factor XIIa without affecting the activity of other coag
    44 n trypsin inhibitor (a specific inhibitor of Factor XIIa without effect on other coagulation factors)
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