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1 allow cleavage by the metalloprotease TACE (TNF-alpha-converting enzyme).
2 ncreases the activity of the metalloprotease TNF-alpha-converting enzyme.
3 ed shedding, but shedding was independent of TNF-alpha-converting enzyme (a disintegrin and metallopr
4 tivation of the metalloprotease TACE/ADAM17 (TNF-alpha-converting enzyme), a previously unknown p53 t
7 n CMV due to an enhanced activity of ADAM17 (TNF-alpha converting enzyme) and matrix metalloprotease
8 phil elastase, tumor necrosis factor [TNF]), TNF-alpha-converting enzyme, and matrix metalloproteinas
9 pparent deficiency in the level of the major TNF-alpha converting enzyme in adipose tissue to account
23 TNF-alpha have centered on the inhibition of TNF-alpha converting enzyme (TACE) through the use of hy
24 ane protein that is enzymatically cleaved by TNF-alpha converting enzyme (TACE) to generate a 17-kDa
27 In the present study, we demonstrate that TNF-alpha converting enzyme (TACE), a disintegrin and me
28 esothelin sheddase activity is mediated by a TNF-alpha converting enzyme (TACE), a member of the matr
29 ly in fibroblasts and monocytes deficient in TNF-alpha converting enzyme (TACE), a sheddase involved
30 F-related apoptosis-inducing ligand (TRAIL), TNF-alpha converting enzyme (TACE), TRAIL receptor (TRAI
36 ase (MAPK) and tumour necrosis factor-alpha (TNF-alpha) converting enzyme (TACE) were also assessed.
44 rophages, by suppressing the activity of the TNF-alpha-converting enzyme (TACE), arguing that MUC1 is
45 lecular mass 26K which can be processed by a TNF-alpha-converting enzyme (TACE), to generate secreted
46 thelial (NCI-H292) cells via metalloprotease TNF-alpha-converting enzyme (TACE)-dependent EGFR activa
47 mucus, and its expression is modulated by a TNF-alpha-converting enzyme (TACE)-EGF receptor pathway
52 vation of the tmTNF cleavage metalloprotease TNF-alpha-converting enzyme via p38 MAP kinase activatio
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