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1                                              2-ME (150 mg/kg p.o., n = 20) inhibited bFGF and VEGF-in
2                                              2-ME activated stress-activated protein kinase (SAPK)/c-
3                                              2-ME ameliorates all pre-eclampsia-like features without
4                                              2-ME exposed cells exhibit Bid cleavage that is accompan
5                                              2-ME was recently reported to inhibit endothelial cell p
6                                              2-ME-induced apoptosis in BPAEC was a time- and concentr
7 ide modes inside the device structure, and a 2-ME+EA interlayer enhances the electron injection and h
8                                 In addition, 2-ME exposure resulted in an increase in mitochondrial m
9                                 In addition, 2-ME inhibited BPAEC migration (IC50 = 0.71 +/- 0.11 mic
10                                Additionally, 2-ME has been shown to inhibit angiogenesis in vitro.
11 1 plays an important protective role against 2-ME-mediated mitochondrial damage by blocking apoptosis
12 e presence and absence of the reducing agent 2-ME indicated that the predicted affinity for 25% of Cy
13                                         Also 2-ME could induce phosphorylation of Bcl-x(L) in G2-M ar
14 or daptomycin in isolates of E. faecalis and 2 ME, 1 for high-level gentamicin resistance and 1 for n
15                       The levels of COMT and 2-ME are significantly lower in women with severe pre-ec
16 ompeting thiol like DTT (dithiothreitol) and 2-ME (2-mercaptoethanol).
17 odel in which antileukemic synergism between 2-ME and HDACIs stems primarily from induction of oxidat
18           Enforced activation of Akt blocked 2-ME/HDACI-mediated mitochondrial injury, caspase activa
19                                         Both 2-ME and l-cysteine also reversed the BSO inhibition of
20 pho-cdc25C (interphase and mitotic forms) by 2-ME(2) treatment correlated with the induction of apopt
21  effectors of apoptotic signaling induced by 2-ME is not known.
22 tion and abrogated M phase arrest induced by 2-ME.
23 ation-dependent mAbs to PrP was inhibited by 2-ME in ELISA, Western blots, and histoblots.
24 ll lines are most sensitive to inhibition by 2-ME.
25 rylation of cdc2 and upregulation of wee1 by 2-ME(2) can be abolished by both extracellular receptor
26  and introducing AR into PC3-M cells confers 2-ME-induced mitotic arrest.
27 thiol-reducing compounds, such as L-cystine, 2-ME, or N-acetyl cysteine, restored FasL expression.
28  by small interfering RNA (siRNA) eliminates 2-ME-induced arrest and introducing AR into PC3-M cells
29                                 Furthermore, 2-ME induced apoptosis in pancreatic cancer cells is mit
30                                     However, 2-ME completely reversed the BSO inhibition of prolifera
31    Fas inhibitors cerulenin or C75 inhibited 2-ME-induced caspase activation, PARP cleavage, apoptosi
32 ous estradiol metabolite 2-medroxyestradiol (2-ME) and histone deacetylase inhibitors (HDACIs) have b
33 atment of these sera with 2-mercaptoethanol (2-ME) reduced, but did not eliminate, their vibriocidal
34 imilar monothiols such as 2-mercaptoethanol (2-ME), that cleavage by DTT exhibits saturation kinetics
35  between IgG anti-LPS and 2-mercaptoethanol (2-ME)-resistant vibriocidal antibodies was 0.81 (P = 0.0
36 at (95 degrees C, 5 min), 2-mercaptoethanol (2-ME, 0.83 %), and l-cysteine (l-Cys, 50 mM) pretreatmen
37 ded: pronase, trypsin, beta-mercaptoethanol (2-ME), and heating to 90 degrees .
38                          2-Methoxyestradiol (2-ME(2)), a promising anticancer drug, induces growth ar
39                          2-Methoxyestradiol (2-ME) is an endogenous metabolite of estradiol-17beta an
40 ntravitreal injection of 2-Methoxyestradiol (2-ME) nanoemulsion in regressing neovascularization of a
41                          2-Methoxyestradiol (2-ME), a new anticancer agent currently in clinical tria
42 iproliferative action of 2-methoxyestradiol (2-ME), an endogenous estrogen metabolite is specific for
43                          2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite of 17beta-estra
44                          2-Methoxyestradiol (2-ME), an endogenous estrogen metabolite which disrupts
45 ere report that low dose 2-methoxyestradiol (2-ME), an endogenous estrogen metabolite, induces mitoti
46 onditions (2.5% oxygen), 2-methoxyestradiol (2-ME), which is a metabolite of estradiol and is generat
47 ting from an absence of 2-methoxyoestradiol (2-ME), a natural metabolite of oestradiol that is elevat
48 al level in the presence of 0.4 and 2 microM 2-ME (n = 3-6), respectively.
49            Neither low-oxygen conditions nor 2-ME alone induces the invasion of cytotrophoblasts in t
50 an important role in the cytotoxic action of 2-ME and that it is possible to use exogenous ROS-produc
51 O(2)- contents and the cytotoxic activity of 2-ME in primary leukemia cells from 50 patients with chr
52 tion, significantly enhanced the activity of 2-ME, even in the CLL cells that were resistant to 2-ME
53 or that affects the antileukemia activity of 2-ME.
54 l of which were disrupted by the addition of 2-ME or DTT, which reduced the single disulfide bond fou
55 mal levels are restored on administration of 2-ME, which also results in the resolution of preeclamps
56 btoxic or marginally toxic concentrations of 2-ME and SAHA or sodium butyrate in diverse human leukem
57 nduced in 21 rats then two concentrations of 2-ME nanoparticles were injected in right eyes of 14 rat
58            Chronic exposure of high doses of 2-ME(2) enhance the accumulation of cells in S and G2/M
59 the present study, we explored the effect of 2-ME on apoptosis in a panel of human pancreatic cancer
60 ed to evaluate the antiangiogenic effects of 2-ME and other microtubule inhibitors such as Taxol, vin
61 ic analysis indicated a novel dual impact of 2-ME(2) on the cell division cycle of prostate cancer ce
62 y be associated with the ultimate impacts of 2-ME(2).
63                    Intravitreal injection of 2-ME (in the two concentrations) caused marked regressio
64 y was undertaken to explore the mechanism of 2-ME effects on endothelial cells, especially whether 2-
65 e antiangiogenic and antitumor properties of 2-ME and Taxol may be crucial in planning clinical appli
66 ts, N-acetylcysteine, reduced glutathione or 2-ME restored both RB phosphorylation and DNA synthesis
67 ed that the ambient 20% oxygen tension (plus 2-ME) is remarkably well suited for immunologic specific
68 lin-like growth factor, or forskolin reduced 2-ME-induced apoptosis.
69 stochemical analysis of BPAEC indicated that 2-ME up-regulated expression of both Fas and Bcl-2.
70 use model for pre-eclampsia and suggest that 2-ME may have utility as a plasma and urine diagnostic m
71      At time 2 (when they developed IM), the 2 ME/CFS groups tended to have more autonomic complaints
72                            We found that the 2 ME/CFS susceptibility HLA alleles above had very weak
73 re was a significant correlation between the 2-ME-induced O(2)- increase and the loss of cell viabili
74 or (SP600125), our studies indicate that the 2-ME(2)-induced upregulation of wee1 and subsequent cdc2
75        MTS-hOGG1-expressing cells exposed to 2-ME showed increased cellular survival and had signific
76  artery endothelial cells (BPAEC) exposed to 2-ME showed morphological (including ultrastructural) fe
77 d hOGG1 (MTS-hOGG1) on HeLa cells exposed to 2-ME.
78  to basal levels at 60 min after exposure to 2-ME.
79 HgCl2-induced modification of fibrillarin to 2-ME, iodoacetamide, and hydrogen peroxide suggested int
80 even in the CLL cells that were resistant to 2-ME alone.
81  indicated that the cell lines responsive to 2-ME could undergo apoptosis either by G2-M arrest (PANC
82  basal O(2)- contents were more sensitive to 2-ME in vitro than those with lower O(2)- contents.
83 PaCa-2, CFPAC-1, PANC-1, or non-sensitive to 2-ME such as Hs 766T.
84 er cell lines, which are either sensitive to 2-ME such as MIA PaCa-2, CFPAC-1, PANC-1, or non-sensiti
85 reatment of human EGP with pronase, trypsin, 2-ME, or heating did not interfere with the ability of h
86 cts on endothelial cells, especially whether 2-ME induces apoptosis, a prime mechanism in tissue remo
87                            We tested whether 2-ME suppresses cytokine-induced angiogenesis in vivo an
88 migration, may be a major mechanism by which 2-ME inhibits angiogenesis.
89 th this rationale, catalysis by CD-0387 with 2-ME as cosubstrate, while less efficient, is not subjec
90 enta are a critical co-stimulator along with 2-ME for the proper invasion of cytotrophoblasts to faci
91 such as arsenic trioxide in combination with 2-ME to enhance the antileukemia activity and to overcom
92 however, low-oxygen conditions combined with 2-ME result in the appropriate invasion of cytotrophobla
93 intracellular redox state by incubation with 2-ME resulted in the secretion of mu(s)-chains, suggesti
94 lecular weight polymers following TGase with 2-ME and heat pretreatment after 3 h of incubation.
95 omal DNA fragmentation in BPAEC treated with 2-ME was identified by agarose gel electrophoresis (DNA
96                               Treatment with 2-ME (75 mg/kg p.o., n = 9) for 1 month suppressed the g
97 ich the low backgrounds after treatment with 2-ME created unusually high signal-to-noise ratios.
98                               Treatment with 2-ME reduced the titers of 17 of 20 patients to < or =50
99  of 2,525 that was removed by treatment with 2-ME.
100                      Notably, treatment with 2-ME/HDACIs resulted in down-regulation of thioredoxin,