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1 rene, pregnenolone-16alpha-carbonitrile, and ciprofibrate.
3 th full-length PPAR alpha in the presence of ciprofibrate, a synthetic ligand, and leukotriene B(4),
4 aximum induction of luciferase expression by ciprofibrate and/or 9-cis-retinoic acid is dependent upo
7 that synthetic PPARalpha ligands Wy-14,643, ciprofibrate, clofibrate, and others induce the nuclear
9 t ML457 cells with monoethylhexyl phthalate, ciprofibrate ethyl ester, and clofibrate also resulted i
10 he PPs Wy-14, 643, monoethylhexyl phthalate, ciprofibrate ethyl ester, and clofibrate suggested that
11 4643, mono-ethylhexyl phthalate, clofibrate, ciprofibrate ethyl ester, and eicosatetraynoic acid each
12 , mono-ethylhexyl phthalate, clofibrate, and ciprofibrate ethyl-ester were found to be potent inducer
14 receptor (PPAR) alpha ligands Wy-14,643 and ciprofibrate increase the Cidea mRNA level in a PPARalph
15 patterns in HCCs from Acox1(-/-) mice and in ciprofibrate-induced HCCs were least similar to those ob
16 inant adenoviral gene transfer abolishes the ciprofibrate-induced over accumulation of apoB-48-carryi
19 challenged with a PPARalpha ligand, such as ciprofibrate or Wy-14,643, the SRC-1(-/-) mice displayed
20 In contrast, treatment of fibroblasts with ciprofibrate or WY14643, PPAR-alpha activators, led to p
23 rt that remnants isolated from the plasma of ciprofibrate-treated apoE-deficient mice bind to murine
25 In the present investigation we report that ciprofibrate treatment causes the down-regulation of hep
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