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1 A, methylenetetrahydrofolate reductase 667T, type 1 plasminogen activator inhibitor 4G/5G, and platel
2 affinity selection with binding activity to type-1 plasminogen activator inhibitor, a trace protein
3 factor beta fails to increase the levels of type 1 plasminogen activator inhibitor and fibronectin s
4 alpain-hydrolyzed Vn revealed that while the type 1 plasminogen activator inhibitor binding activity
5 ation of native Vn, or its complexation with type 1 plasminogen activator inhibitor, exposed the cell
6 showed a codistribution of multimeric Vn and type 1 plasminogen activator inhibitor in alpha-granule-
7 rin serves as a template for the assembly of type 1 plasminogen activator inhibitor-induced disulfide
8 l microcirculation and that local changes in type 1 plasminogen activator inhibitor (PAI-1) gene expr
10 duced lung fibrosis, increased expression of type 1 plasminogen activator inhibitor (PAI-1) is associ
12 hypothesized that lower protein C and higher type 1 plasminogen activator inhibitor (PAI-1) levels in
15 s TGF-beta transcriptional activation of the type-1 plasminogen activator inhibitor (PAI-1) gene in a
16 -fold increase in the rate of degradation of type-1 plasminogen activator inhibitor (PAI-1) mRNA.
17 ble to increased concentrations in plasma of type-1 plasminogen activator inhibitor (PAI-1), the prim
19 -fold increase in the rate of degradation of type-1 plasminogen activator-inhibitor (PAI-1) mRNA.
20 vel TGF-beta-responsive element in the human type 1 plasminogen activator inhibitor promoter that is
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