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1 icant reduction of its endogenous inhibitor, tissue inhibitor of metalloproteinase-3.
2 evels, but did not affect mRNA levels of the tissue inhibitor of metalloproteinase-3.
5 ssion events by delivering molecules such as tissue inhibitor of metalloproteinase-3 and angiopoietin
6 ed expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-3, and elastin.
7 ed expression of predicted miR-181b targets, tissue inhibitor of metalloproteinase-3, and elastin.
8 yl oxidase, adamalysin metalloproteinase-17, tissue inhibitors of metalloproteinase-3, c-Met and CXCR
9 afforded by miR-181b inhibition are largely tissue inhibitor of metalloproteinase-3 dependent, while
10 l-specific molecule-1, 5'-ecto-nucleotidase, tissue inhibitor of metalloproteinase-3, epidermal growt
11 To investigate whether miR-181b regulates tissue inhibitor of metalloproteinase-3 expression and a
12 hat miR-181b negatively regulates macrophage tissue inhibitor of metalloproteinase-3 expression and v
13 ive CXCR2 ligand GROalpha (10 ng/ml) induced tissue inhibitor of metalloproteinase-3 expression, mark
14 Kop protease inhibitor, matrix gla protein, tissue inhibitor of metalloproteinase 3, folate receptor
15 ase-specific inhibitors BB-94 and GM6001 and tissue inhibitor of metalloproteinase-3 partially inhibi
16 ith pan-metalloproteinase inhibitors or with tissue inhibitors of metalloproteinase-3 reduced neurite
17 We have cloned the cDNA encoding the rat tissue inhibitor of metalloproteinase 3 (TIMP-3) by a PC
18 ic response in human articular chondrocytes, tissue inhibitor of metalloproteinase 3 (TIMP-3) inducti
20 nes retinoic acid receptor beta-2 (RARbeta), tissue inhibitor of metalloproteinase 3 (TIMP-3), p16INK
21 ted involution in wild-type mice, but not in tissue inhibitor of metalloproteinase 3 (TIMP-3)-deficie
23 se inhibitor-2 (TAPI-2), phenanthroline, and tissue inhibitor of metalloproteinase-3 (TIMP-3) but not
24 ase of the macula caused by mutations in the tissue inhibitor of metalloproteinase-3 (TIMP-3) gene.
25 of blindness, is caused by mutations in the tissue inhibitor of metalloproteinase-3 (TIMP-3) gene.
28 ecanase activity with monoclonal antibodies, tissue inhibitor of metalloproteinases 3 (TIMP-3), and c
29 recognized aggrecanases and their inhibitor, tissue inhibitor of metalloproteinases 3 (TIMP-3), in hu
35 ddition, CaPPS increased cartilage levels of tissue inhibitor of metalloproteinases-3 (TIMP-3), an en
38 uble Pref-1A is inhibited by TAPI-0 and by a tissue inhibitor of metalloproteinase-3, TIMP-3, that ca
39 ically, d-flow-induced miR-712 downregulates tissue inhibitor of metalloproteinase 3 (TIMP3) expressi
41 1 (ADAMTS1) and downregulated its inhibitor, tissue inhibitor of metalloproteinase 3 (TIMP3) in respo
43 in natural regulator of TACE activity is the tissue inhibitor of metalloproteinase 3 (Timp3), we hypo
44 ogenic effects by upregulating expression of tissue inhibitor of metalloproteinase-3 (TIMP3) in a P53
55 e-wide association study; the locus near the tissue inhibitor of metalloproteinase 3 was corroborated
56 ents with active AAV, but those of ADAM10 or tissue inhibitor of metalloproteinases 3, which inhibits
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