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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.
3                                         3, 3-Diindolylmethane-14 (DIM-14), a novel lipophilic derivat
4                                    DIM (3,3'-diindolylmethane), a small molecule compound, is a propo
5         In addition, we discovered that 3,3'-diindolylmethane, a dietary molecule from cruciferous ve
6          Because other methylene-substituted diindolylmethane analogues have been shown to transactiv
7                                         3,3'-Diindolylmethane and decanoic acid acted as strong posit
8 ncentrations of either decanoic acid or 3,3'-diindolylmethane and was not affected adversely by mutat
9        Together, these findings suggest that diindolylmethanes are a new class of compounds that sele
10 onist actions of both decanoic acid and 3,3'-diindolylmethane at GPR84.
11                                         3,3'-Diindolylmethanes bearing small lipophilic residues at t
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-(
15                                     Selected diindolylmethane compounds (C-DIMs) have been shown to a
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
19              We synthesized a broad range of diindolylmethane derivatives by condensation of indoles
20   Thus, this series of methylene-substituted diindolylmethane derivatives simultaneously activate mul
21  deficient rho(0) MCF-7 cells, in which 3,3'-diindolylmethane did not stimulate ROS production.
22                            Rosiglitazone and diindolylmethane (DIM) analogues did not affect expressi
23             We also find that the diindoles, diindolylmethane (DIM) and diindolylethane (DIE) selecti
24 rmylindolo-[3,2-b]carbazole (FICZ), and 3-3'-diindolylmethane (DIM) and then analyzed with a combinat
25             Indole-3-carbinol (I3C) and 3,3'-diindolylmethane (DIM) are two bioactive compounds from
26 nzo-p-dioxin (TCDD) (reference) or 25 microM diindolylmethane (DIM) as AhR agonists in MCF-7 cells.
27                                         3,3'-Diindolylmethane (DIM) has been known to have cancer che
28                                         3,3'-Diindolylmethane (DIM) has been shown to repress neovasc
29              We evaluated the effect of 3,3'-diindolylmethane (DIM) in ovarian cancer cells.
30 oliferative and proapoptotic effects of 3,3'-diindolylmethane (DIM) in prostate cancer cells.
31                                         3,3'-Diindolylmethane (DIM) is a major digestive product of i
32                                         3,3'-Diindolylmethane (DIM) is a promising anticancer agent d
33  The indole-3-carbinol (I3C) metabolite 3,3'-diindolylmethane (DIM) is a proposed cancer prevention a
34                                         3,3'-Diindolylmethane (DIM) is an anticancer agent that induc
35 phane (SFN) and indole-3-carbinol (I3C)/3,3'-diindolylmethane (DIM) on breast cancer risk, prognosis,
36 eatment of cells with "natural agents" [3,3'-diindolylmethane (DIM) or isoflavone] could affect the e
37 s major acid-catalyzed reaction product 3,3'-diindolylmethane (DIM) showed anticancer activity mediat
38 liferative and pro-apoptotic effects of 3,3'-diindolylmethane (DIM) through regulation of Akt and and
39                                Finally, 3,3'-Diindolylmethane (DIM), a known chemoprevention agent, i
40                                         3,3'-Diindolylmethane (DIM), a major in vivo acid-catalyzed c
41                                         3,3'-Diindolylmethane (DIM), a natural autolytic product in p
42 sitization of pancreatic cancer cells by 3,3-diindolylmethane (DIM), a natural compound that can be e
43              Furthermore, we found that 3,3'-diindolylmethane (DIM), a vegetable autolysis product, p
44 es, and its major condensation product, 3,3'-diindolylmethane (DIM), against lung tumorigenesis induc
45  cancer cells by different concentrations of diindolylmethane (DIM), an active ingredient of crucifer
46  in vitro gastrointestinal digestion for 3,3-diindolylmethane (DIM), indole-3-carbinol (I3C) and sulf
47 hR ligands (indole-3-carbinol [I3C] and 3,3'-diindolylmethane [DIM]) and an endogenous AhR ligand, 6-
48 ed that I3C, but not its natural dimer, 3,3'-diindolylmethane, disrupts proteolytic processing of the
49 ate the molecular mechanism(s) by which 3,3'-diindolylmethane exerts its effects on breast cancer cel
50 uced p21 overexpression, we showed that 3,3'-diindolylmethane failed to induce p21 overexpression in
51         The anti-inflammatory effect of 3,3'-diindolylmethane in RAW264.7 cells was shown to be parti
52 s studies in our laboratory showed that 3,3'-diindolylmethane induced a G(1) cell cycle arrest in hum
53 , antioxidants significantly attenuated 3,3'-diindolylmethane-induced activation of p38 and JNK and i
54 survivin by cDNA transfection abrogated 3,3'-diindolylmethane-induced cell growth inhibition and apop
55 NH(2)-terminal kinase (JNK) pathways in 3,3'-diindolylmethane-induced p21 mRNA transcription.
56   To further support the role of ROS in 3,3'-diindolylmethane-induced p21 overexpression, we showed t
57 f enhanced mitochondrial ROS release in 3,3'-diindolylmethane-induced p21 up-regulation in human brea
58 ple molecular approaches and found that 3,3'-diindolylmethane inhibited cell growth and induced apopt
59         We show for the first time that 3,3'-diindolylmethane is a strong mitochondrial H(+)-ATPase i
60                                         3,3'-Diindolylmethane, one of the active products derived fro
61 trast, the chemopreventative AHR ligand 3,3'-diindolylmethane promotes AHR nuclear translocation and
62 rile, indole-3-carbinol, ascorbigen and 3,3'-diindolylmethane released from glucobrassicin and 4-meth
63 her and analysis showed the affinity of 3,3'-diindolylmethane to be at least 100 fold higher.
64 found a total of 1,238 genes altered in 3,3'-diindolylmethane-treated cells, among which 550 genes we
65                                         3,3'-Diindolylmethane treatment induced hyperpolarization of
66 urvivin by small interfering RNA before 3,3'-diindolylmethane treatment resulted in enhanced cell gro
67                               Recently, 3,3'-diindolylmethane was identified as a heterocyclic, nonli