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1 re critical for the biological activities of emodin.
2      Subsequent in vitro validation revealed emodin (1) and physcion (2) to be potent antimalarial ca
3                                              Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is an ac
4 vehicle-treated groups) after treatment with emodin (6 days at 60 mg/kg per day) and by approximately
5                           Here, we show that emodin, a natural compound, can directly target AR to su
6 cin biosynthesis after the administration of emodin, a precursor of hypericin.
7               Recently, we demonstrated that emodin, a tyrosine kinase inhibitor, suppresses HER-2/ne
8  that clinically achievable doses of DHA and emodin allowed for reduced arsenic concentrations by 100
9 o well-known secondary metabolites including emodin, aloe-emodin, B-sitosterol and rutin.
10 o well-known secondary metabolites including emodin, aloe-emodin, beta-sitosterol and rutin.
11     HyH product inhibition was observed with emodin analogues, rhein, rhein methyl ester, and DNA3-55
12 tudies, the relative binding energies of the emodin and aloe-emodin derivatives to human serum albumi
13 synthesized from the isolated anthraquinones emodin and aloe-emodin of Rhubarb to increase the bioact
14 synthesized from the isolated anthraquinones emodin and aloe-emodin of Rhubarb to increase the bioact
15 ionale for combined use of As/IFN-alpha with emodin and DHA in patients with ATL refractory to conven
16 ide and interferon alpha (As/IFN-alpha) with emodin and DHA on cell-cycle arrest and cell death of HT
17 rmed 3T3 cells, we also investigated whether emodin and DK-V-47 can inhibit malignant transformation
18 nhibition of p185neu tyrosine kinase by both emodin and DK-V-47 is capable of suppressing the HER-2/n
19 se CK2 (formerly, casein kinase II), such as emodin and DRB, were able to duplicate the effects of H7
20 n the chemical structure and the activity of emodin and nine derivatives, and identified that one met
21 on of anthraquinones to xanthones accumulate emodins and are delayed in maturation and growth of frui
22 ted with LPS/IFNgamma or IL4 with or without emodin, and the effects of emodin on gene transcription,
23                 Thioflavin T, clioquinol and emodin are promising leads in AD and PD research, whose
24 ffect and justifies further investigation of emodin as a therapeutic and preventive agent for prostat
25 secondary metabolites including emodin, aloe-emodin, B-sitosterol and rutin.
26 secondary metabolites including emodin, aloe-emodin, beta-sitosterol and rutin.
27                                We found that emodin bidirectionally tunes the induction of LPS/IFNgam
28                                 Reduction of emodin by sodium dithionite resulted in the formation of
29  and that tyrosine kinase inhibitors such as emodin can sensitize these cells to chemotherapeutic dru
30 nd (2) whether the tyrosine kinase inhibitor emodin can sensitize these cells to chemotherapeutic dru
31 sing lung cancer cells, whereas low doses of emodin, cisplatin, doxorubicin, or VP16 alone had only m
32  dimerization dramatically increases nataloe-emodin cytotoxicity against mammalian cell lines.
33                                              Emodin decreased the association of AR and heat shock pr
34                                We found that emodin decreased tyrosine phosphorylation of HER-2/neu a
35                                         Aloe-emodin derivative with N(a)Fmoc-l-Lys shows the highest
36                                         Aloe-emodin derivative with N(alpha)Fmoc-l-Lys shows the high
37 tive binding energies of the emodin and aloe-emodin derivatives to human serum albumin ranged from -7
38                                              Emodin did not chemically modify NF-kappaB subunits but
39                  The asymmetric reduction of emodin hydroquinone to (R)-3,8,9,10-tetrahydroxy-6-methy
40  first (nonenzymatic) reduction of emodin to emodin hydroquinone, for example with sodium dithionite,
41  in the formation of two tautomeric forms of emodin hydroquinone.
42 re chrysophanol in R. alaternus (3.14 mg/g), emodin in R. pumila (0.339 mg/g), and physcion in R. fal
43 -9-anthrone (DK-V-47) is more effective than emodin in repressing the tyrosine phosphorylation of p18
44 contents of physcion, chrysophanol, and aloe-emodin in rhubarb were determined to be 0.22%, 1.0%, and
45 determining physcion, chrysophanol, and aloe-emodin in rhubarb.
46    We found that DK-V-47 is more potent than emodin in suppressing transformation phenotypes of activ
47              Pretreatment of EC for 1 h with emodin inhibited both monocyte-EC attachment and express
48                                 Furthermore, emodin inhibited the removal of H3K27 trimethylation (H3
49  TNF activated NF-kappaB; preincubation with emodin inhibited this activation in a dose- and time-dep
50                                              Emodin is a Chinese herb-derived compound and has shown
51                  These results indicate that emodin is a potent inhibitor of NF-kappaB activation and
52         In conclusion, our data suggest that emodin is uniquely able to suppress the excessive respon
53   Our work indicates a new mechanism for the emodin-mediated anticancer effect and justifies further
54                                     Thereby, emodin modulates macrophage phagocytosis, migration, and
55  the isolated anthraquinones emodin and aloe-emodin of Rhubarb to increase the bioactivities.
56  the isolated anthraquinones emodin and aloe-emodin of Rhubarb to increase the bioactivities.
57 4 with or without emodin, and the effects of emodin on gene transcription, cell signaling pathways, a
58 present study we investigated the effects of emodin on the activation of NF-kappaB in human umbelical
59 ttachment of leukocytes to EC, the effect of emodin on the adhesion of monocytes to EC and the expres
60                     Octreotide combined with emodin or 4,5,6,7-tetrabromobenzotriazole blocked mouse
61             A combination of CK2 inhibitors, emodin or 4,5,6,7-tetrabromobenzotriazole, with octreoti
62 herapeutic implications of the use of either emodin or DK-V-47 to target HER-2/neu-overexpressing can
63 fulvin, an asymmetrical homodimer of nataloe-emodin produced by the fungus Cladosporium fulvum A gene
64                                              Emodin represses fruiting body and resting structure for
65                We have previously shown that emodin suppresses tyrosine kinase activity of HER-2/neu-
66 0 ClaM catalyzes the dimerization of nataloe-emodin to cladofulvin.
67        The first (nonenzymatic) reduction of emodin to emodin hydroquinone, for example with sodium d
68 monstrate a direct and complex conversion of emodin to HyH that is solely catalyzed by Hyp-1, a Bet.v
69 nd were further screened for biosynthesis of emodin to hypericin, which resulted in an 84.6% conversi
70      In this study, we tested the ability of emodin to modulate the macrophage response to both M1 an
71                                              Emodin treatment resulted in repressing androgen-depende
72 t Hyp-1 protein was able to convert HyH from emodin under in vitro conditions.
73  bound with NADPH or NADP+ and the inhibitor emodin were solved with the wild type and P94L mutant of
74                                 In contrast, emodin, which blocks phosphorylation of her2/neu by here
75  compound is decarboxylated by ClaH to yield emodin, which is then converted to chrysophanol hydroqui
76            Further, modification of the aloe-emodin with both the ethynyl and the N(a)Fmoc-l-Lys grou
77            Further, modification of the aloe-emodin with both the ethynyl and the N(alpha)Fmoc-l-Lys
78              Furthermore, the combination of emodin with cisplatin, doxorubicin or etoposide (VP16) s