ライフサイエンスコーパス: 2ME

1 2ME induced apoptosis in these cells in a dose-dependent

2 2ME(2) also suppresses osteoclast differentiation and in

3 2ME(2) inhibited tumor growth in soft tissue, metastasis

4 PbI(3) exhibits 10x higher solubility in 30% 2ME in GBL than in 2ME alone and 40% higher solubility t

5 Equivalent binding of [3H]2ME occurred when the drug was added to preformed polyme

6 ded to preformed polymer, but binding of [3H]2ME to polymer was not readily inhibited by colchicine s

7 Significant amounts of [3H]2ME were also incorporated into microtubule polymer form

8 el protofilaments, increasing amounts of [3H]2ME were incorporated into polymer, reaching near-stoich

9 The [3H]2ME binds avidly to tubulin even on ice, and it is readi

10 We have now examined interactions of [4-3H]-2ME with unpolymerized tubulin and polymer.

11 Although 2ME(2) significantly reduced tumor growth at late stages

12 However, although 2ME(2) reduced the number of MIN lesions in the preventi

13 gic or genetic (e.g. siRNA) means attenuated 2ME-induced mitochondrial injury, XIAP and Mcl-1 downreg

14 action rate is observed for the bifunctional 2ME (4 abstraction positions) over n-butanol (5 abstract

15 the response to oxidative stress induced by 2ME.

16 t Id-1 expression is negatively regulated by 2ME(2), which may be an additional mechanism for the ant

17 Conversely, 2ME lethality was potentiated by the phosphatidylinosito

18 o these differences in apparent affinity for 2ME are unknown, but presumably interaction of the estro

19 However, for 2ME the energy barriers increase in the order alpha < be

20 gen receptors (ERs) as molecular targets for 2ME(2).

21 gy and accelerated tumor growth may occur if 2ME(2) is administered in a prevention setting for prolo

22 higher solubility in 30% 2ME in GBL than in 2ME alone and 40% higher solubility than in GBL alone at

23 ecyl sulfate (SDS) and beta-mercaptoethanol (2ME), suggesting the recognition of nonlinear or conform

24 2-Methoxyestradiol (2ME(2)) is an endogenous metabolite of 17beta-estradiol

25 2-Methoxyestradiol (2ME(2)), a metabolite of 17-beta-estradiol, inhibits ang

26 2-Methoxyestradiol (2ME(2)), a physiologic metabolite of 17beta-estradiol (e

27 2-Methoxyestradiol (2ME) is an endogenous mammalian catabolite of estradiol

28 The effects of 2-Methoxyestradiol (2ME)-induced apoptosis was examined in human leukemia ce

29 oxidation of bifunctional 2-Methoxyethanol (2ME) biofuel using methyl radical was introduced.

30 ma-butyrolactone (GBL) and 2-methoxyethanol (2ME), a phenomenon where FAPbI(3) shows higher solubilit

31 ear-stoichiometry with tubulin at 100 microM 2ME.

32 ot inhibit the antiproliferative activity of 2ME(2).

33 sts, and we demonstrate that the affinity of 2ME(2) for ERbeta is even lower.

34 l mechanism for the antiangiogenic effect of 2ME(2).

35 analyzed the tumor stage-specific effects of 2ME(2) in the C3(1)/Tag transgenic mouse model for breas

36 ese findings suggest a hierarchical model of 2ME-related apoptosis induction in human leukemia cells

37 iferative activity of ICI 182,780 but not of 2ME(2).

38 ce for various channels for the oxidation of 2ME was studied at density function theory (M06-2X) and

39 f organic compounds, from different sites of 2ME were examined.

40 active myristolated Akt construct prevented 2ME-mediated mitochondrial injury, XIAP and Mcl-1 downre

41 was significantly reduced in mice receiving 2ME(2).

42 In the latter study, 2ME(2) (10, 25, and 50 mg/kg/d) treatment began on the s

43 Our data support the conclusion that 2ME(2) could be an important new therapy in the arsenal

44 We confirm that 2ME(2) has a lower binding affinity for ERalpha as compa

45 Collectively, these results suggest that 2ME(2) is distinct among estradiol metabolites because o

46 In vitro 2ME(2) inhibits a large variety of tumor and nontumor ce

47 In vitro, 2ME(2) repressed osteoclast number by inducing apoptosis

48 these observations, we have examined whether 2ME(2) could effectively target metastasis to bone, oste

49 ose of this study was to investigate whether 2ME(2) is able to engage ERs as an agonist and whether i

50 enzyme inhibitor, at concentrations at which 2ME(2) interacts with ERalpha in an in vitro binding ass

51 s induction in human leukemia cells in which 2ME-induced oxidative injury represents a primary event

52 cystic tumor formation in mice treated with 2ME(2) at early ages are consistent with an impaired ang

53 ption of the hydrogen bonding network within 2ME, allowing its hydroxyl and ether groups to interact