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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
5                          AEC pretreated with mevastatin, a specific inhibitor of prenylation, or tran
6                     We conclude that topical mevastatin accelerates wound closure by promoting epithe
7                                              Mevastatin also caused apoptosis in both wild-type and p
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
10                                              Mevastatin, an inhibitor of cholesterol synthesis, inhib
11 erol and sphingomyelin synthesis inhibitors (mevastatin and myriocin, respectively), suggesting that
12                                         Both mevastatin and simvastatin caused a concentration- and t
13 bserved after treatments with brefeldin A or mevastatin and when the conserved isoprenylation sequenc
14                    The statins mevinolin and mevastatin are weak inhibitors of L. monocytogenes HMG-C
15                                              Mevastatin arrested HCT116 colon cancer cells at the G1/
16                                              Mevastatin blocked cholesterol accumulation in injured H
17                                 We find that mevastatin does not appear to be a substrate for hCE1, a
18  rosuvastatin = simvastatin > atorvastatin = mevastatin > pravastatin, which is similar to the known
19                                              Mevastatin increased eNOS mRNA and protein levels by 305
20                 In p27Kip1-deficient PASMCs, mevastatin induced a greater reduction of cyclin E prote
21                                We found that mevastatin induced G1 arrest and decreased DNA synthesis
22 eletion and mutational analyses suggest that mevastatin induced KLF2 promoter activity through a sing
23 ly rescued primary rat cortical neurons from mevastatin-induced neurotoxicity.
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
26          Using RNA interference we show that mevastatin inhibits cdk2 activity despite lack of induct
27                   These results suggest that mevastatin inhibits cdk2 activity in PC3 cells through t
28                                              Mevastatin is an inhibitor of 3-hydroxy-3-methylglutaryl
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
31                 Treatment of these AMLs with mevastatin or zaragozic acid (which inhibits cholesterol
32                                 Importantly, mevastatin reversed c-Myc overexpression in DFUs.
33 onstrate that the naturally occurring statin mevastatin reverses FPP's effects and promotes healing b
34 lonate or GGPP, but not FPP or LDL, reversed mevastatin's effects.
35 wever, in PASMCs lacking functional p27Kip1, mevastatin still decreased cyclin E kinase activity, cau
36                             Of note, topical mevastatin stimulated epithelialization and angiogenesis
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
39                  Treatment of 293 cells with mevastatin to deplete cellular mevalonate resulted in an
40 n of KLF2 strongly attenuated the ability of mevastatin to increase eNOS and thrombomodulin accumulat
41 important role for p27Kip1 in the ability of mevastatin to induce G1 arrest.
42                 Phosphorylation of cdk2 from mevastatin-treated cells with exogenous cyclin-dependent
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
45         In a prostate cancer cell line, PC3, mevastatin treatment led to elevated levels of p21 and c
46       Apoptosis induced by bisphosphonate or mevastatin was found to be dependent on protein synthesi
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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