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1 84 but so also can molecules related to 3,3'-diindolylmethane.
2 the action of decanoic acid but not of 3,3'-diindolylmethane.
8 ncentrations of either decanoic acid or 3,3'-diindolylmethane and was not affected adversely by mutat
12 studies on a series of methylene-substituted diindolylmethanes (C-DIM) have identified 1,1-bis(3'-ind
13 tion of Egr-1/NAG-1 by methylene-substituted diindolylmethanes (C-DIMs) was phosphatidylinositol 3-ki
14 te the efficacy of a novel anti-inflammatory diindolylmethane class compound, 1,1-bis(3'-indolyl)-1-(
16 ults suggest that targeting survivin by 3,3'-diindolylmethane could be a new and novel approach for t
17 n-regulation of survivin as observed by 3,3'-diindolylmethane could be an important approach for the
18 tion of a newly synthesized ring-substituted diindolylmethane derivative, 1,1-bis[3'-(5-methoxyindoly
20 Thus, this series of methylene-substituted diindolylmethane derivatives simultaneously activate mul
23 rmylindolo-[3,2-b]carbazole (FICZ), and 3-3'-diindolylmethane (DIM) and then analyzed with a combinat
25 nzo-p-dioxin (TCDD) (reference) or 25 microM diindolylmethane (DIM) as AhR agonists in MCF-7 cells.
32 The indole-3-carbinol (I3C) metabolite 3,3'-diindolylmethane (DIM) is a proposed cancer prevention a
34 eatment of cells with "natural agents" [3,3'-diindolylmethane (DIM) or isoflavone] could affect the e
35 s major acid-catalyzed reaction product 3,3'-diindolylmethane (DIM) showed anticancer activity mediat
36 liferative and pro-apoptotic effects of 3,3'-diindolylmethane (DIM) through regulation of Akt and and
40 sitization of pancreatic cancer cells by 3,3-diindolylmethane (DIM), a natural compound that can be e
42 es, and its major condensation product, 3,3'-diindolylmethane (DIM), against lung tumorigenesis induc
43 cancer cells by different concentrations of diindolylmethane (DIM), an active ingredient of crucifer
44 hR ligands (indole-3-carbinol [I3C] and 3,3'-diindolylmethane [DIM]) and an endogenous AhR ligand, 6-
45 ed that I3C, but not its natural dimer, 3,3'-diindolylmethane, disrupts proteolytic processing of the
46 ate the molecular mechanism(s) by which 3,3'-diindolylmethane exerts its effects on breast cancer cel
47 uced p21 overexpression, we showed that 3,3'-diindolylmethane failed to induce p21 overexpression in
49 s studies in our laboratory showed that 3,3'-diindolylmethane induced a G(1) cell cycle arrest in hum
50 , antioxidants significantly attenuated 3,3'-diindolylmethane-induced activation of p38 and JNK and i
51 survivin by cDNA transfection abrogated 3,3'-diindolylmethane-induced cell growth inhibition and apop
53 To further support the role of ROS in 3,3'-diindolylmethane-induced p21 overexpression, we showed t
54 f enhanced mitochondrial ROS release in 3,3'-diindolylmethane-induced p21 up-regulation in human brea
55 ple molecular approaches and found that 3,3'-diindolylmethane inhibited cell growth and induced apopt
58 trast, the chemopreventative AHR ligand 3,3'-diindolylmethane promotes AHR nuclear translocation and
59 rile, indole-3-carbinol, ascorbigen and 3,3'-diindolylmethane released from glucobrassicin and 4-meth
61 found a total of 1,238 genes altered in 3,3'-diindolylmethane-treated cells, among which 550 genes we
63 urvivin by small interfering RNA before 3,3'-diindolylmethane treatment resulted in enhanced cell gro
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