ライフサイエンスコーパス: emodin

1 re critical for the biological activities of emodin.

2 Emodin (3-methyl-1,6,8-trihydroxyanthraquinone) is an ac

3 vehicle-treated groups) after treatment with emodin (6 days at 60 mg/kg per day) and by approximately

4 Here, we show that emodin, a natural compound, can directly target AR to su

5 cin biosynthesis after the administration of emodin, a precursor of hypericin.

6 Recently, we demonstrated that emodin, a tyrosine kinase inhibitor, suppresses HER-2/ne

7 that clinically achievable doses of DHA and emodin allowed for reduced arsenic concentrations by 100

8 HyH product inhibition was observed with emodin analogues, rhein, rhein methyl ester, and DNA3-55

9 ionale for combined use of As/IFN-alpha with emodin and DHA in patients with ATL refractory to conven

10 ide and interferon alpha (As/IFN-alpha) with emodin and DHA on cell-cycle arrest and cell death of HT

11 rmed 3T3 cells, we also investigated whether emodin and DK-V-47 can inhibit malignant transformation

12 nhibition of p185neu tyrosine kinase by both emodin and DK-V-47 is capable of suppressing the HER-2/n

13 se CK2 (formerly, casein kinase II), such as emodin and DRB, were able to duplicate the effects of H7

14 n the chemical structure and the activity of emodin and nine derivatives, and identified that one met

15 ted with LPS/IFNgamma or IL4 with or without emodin, and the effects of emodin on gene transcription,

16 ffect and justifies further investigation of emodin as a therapeutic and preventive agent for prostat

17 We found that emodin bidirectionally tunes the induction of LPS/IFNgam

18 Reduction of emodin by sodium dithionite resulted in the formation of

19 and that tyrosine kinase inhibitors such as emodin can sensitize these cells to chemotherapeutic dru

20 nd (2) whether the tyrosine kinase inhibitor emodin can sensitize these cells to chemotherapeutic dru

21 sing lung cancer cells, whereas low doses of emodin, cisplatin, doxorubicin, or VP16 alone had only m

22 dimerization dramatically increases nataloe-emodin cytotoxicity against mammalian cell lines.

23 Emodin decreased the association of AR and heat shock pr

24 We found that emodin decreased tyrosine phosphorylation of HER-2/neu a

25 Emodin did not chemically modify NF-kappaB subunits but

26 The asymmetric reduction of emodin hydroquinone to (R)-3,8,9,10-tetrahydroxy-6-methy

27 first (nonenzymatic) reduction of emodin to emodin hydroquinone, for example with sodium dithionite,

28 in the formation of two tautomeric forms of emodin hydroquinone.

29 re chrysophanol in R. alaternus (3.14 mg/g), emodin in R. pumila (0.339 mg/g), and physcion in R. fal

30 -9-anthrone (DK-V-47) is more effective than emodin in repressing the tyrosine phosphorylation of p18

31 contents of physcion, chrysophanol, and aloe-emodin in rhubarb were determined to be 0.22%, 1.0%, and

32 determining physcion, chrysophanol, and aloe-emodin in rhubarb.

33 We found that DK-V-47 is more potent than emodin in suppressing transformation phenotypes of activ

34 Pretreatment of EC for 1 h with emodin inhibited both monocyte-EC attachment and express

35 Furthermore, emodin inhibited the removal of H3K27 trimethylation (H3

36 TNF activated NF-kappaB; preincubation with emodin inhibited this activation in a dose- and time-dep

37 Emodin is a Chinese herb-derived compound and has shown

38 These results indicate that emodin is a potent inhibitor of NF-kappaB activation and

39 In conclusion, our data suggest that emodin is uniquely able to suppress the excessive respon

40 Our work indicates a new mechanism for the emodin-mediated anticancer effect and justifies further

41 Thereby, emodin modulates macrophage phagocytosis, migration, and

42 4 with or without emodin, and the effects of emodin on gene transcription, cell signaling pathways, a

43 present study we investigated the effects of emodin on the activation of NF-kappaB in human umbelical

44 ttachment of leukocytes to EC, the effect of emodin on the adhesion of monocytes to EC and the expres

45 Octreotide combined with emodin or 4,5,6,7-tetrabromobenzotriazole blocked mouse

46 A combination of CK2 inhibitors, emodin or 4,5,6,7-tetrabromobenzotriazole, with octreoti

47 herapeutic implications of the use of either emodin or DK-V-47 to target HER-2/neu-overexpressing can

48 fulvin, an asymmetrical homodimer of nataloe-emodin produced by the fungus Cladosporium fulvum A gene

49 We have previously shown that emodin suppresses tyrosine kinase activity of HER-2/neu-

50 0 ClaM catalyzes the dimerization of nataloe-emodin to cladofulvin.

51 The first (nonenzymatic) reduction of emodin to emodin hydroquinone, for example with sodium d

52 monstrate a direct and complex conversion of emodin to HyH that is solely catalyzed by Hyp-1, a Bet.v

53 nd were further screened for biosynthesis of emodin to hypericin, which resulted in an 84.6% conversi

54 In this study, we tested the ability of emodin to modulate the macrophage response to both M1 an

55 Emodin treatment resulted in repressing androgen-depende

56 t Hyp-1 protein was able to convert HyH from emodin under in vitro conditions.

57 bound with NADPH or NADP+ and the inhibitor emodin were solved with the wild type and P94L mutant of

58 In contrast, emodin, which blocks phosphorylation of her2/neu by here

59 compound is decarboxylated by ClaH to yield emodin, which is then converted to chrysophanol hydroqui

60 Furthermore, the combination of emodin with cisplatin, doxorubicin or etoposide (VP16) s