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1 was abrogated by simultaneous treatment with mevastatin.
2 continued to proliferate in the presence of mevastatin.
3 rol depletion by methyl-beta-cyclodextrin or mevastatin.
4 reated with the HMG-CoA reductase inhibitor, mevastatin (1-10 microM), in the presence of L-mevalonat
8 d epithelialization and angiogenesis in vivo Mevastatin also reversed FPP-mediated induction of the G
9 trin, which reversibly binds cholesterol, or mevastatin, an inhibitor of cholesterol biosynthesis, to
11 erol and sphingomyelin synthesis inhibitors (mevastatin and myriocin, respectively), suggesting that
13 bserved after treatments with brefeldin A or mevastatin and when the conserved isoprenylation sequenc
18 rosuvastatin = simvastatin > atorvastatin = mevastatin > pravastatin, which is similar to the known
22 eletion and mutational analyses suggest that mevastatin induced KLF2 promoter activity through a sing
24 ured cortisol levels by ELISA and found that mevastatin inhibited cortisol synthesis in keratinocytes
25 [35S]GTPgammaS-binding assays revealed that mevastatin inhibited Rho membrane translocation and GTP
29 G1/S arrest of HCT116 colon cancer cells by mevastatin, its mode of action was more complicated than
30 of this study was to determine the effect of mevastatin on DNA synthesis, cell cycle progression, and
33 onstrate that the naturally occurring statin mevastatin reverses FPP's effects and promotes healing b
35 wever, in PASMCs lacking functional p27Kip1, mevastatin still decreased cyclin E kinase activity, cau
37 ctivating kinase, Cak), was not inhibited by mevastatin, suggesting either that a different CAK is re
38 complexes with the cholesterol-lowering drug mevastatin, the breast cancer drug tamoxifen, the fatty
40 n of KLF2 strongly attenuated the ability of mevastatin to increase eNOS and thrombomodulin accumulat
43 bition of both pathways simultaneously using mevastatin-treated Ldlr(-/-) cells did inhibit forskolin
44 cells, or of cholesterol biosynthesis, using mevastatin-treated WT cells, failed to inhibit matrix mi
47 oxy-3-methylglutaryl-CoA-reductase inhibitor mevastatin, which blocks FPP formation, not only promote
48 bset of patients and grown in 0.5% serum and mevastatin with increasing amounts of recombinant PCSK9.
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