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1 ment in cells grown in the presence of alpha-difluoromethylornithine.
2 re potent inhibitor of the enzyme than alpha-difluoromethylornithine.
3 xogenous putrescine in the presence of alpha-difluoromethylornithine.
4 y preventing putrescine formation with alpha-difluoromethylornithine.
5 on of Xenopus oocytes injected with 50 nl of difluoromethylornithine (5 mM) and methylglyoxal bis(gua
6 ivation is polyamine dependent because alpha-difluoromethylornithine, a specific inhibitor of ODC act
11 dition, in vivo inhibition of ODC with alpha-difluoromethylornithine also exacerbated the colitis.
14 depletion of cellular polyamines with alpha-difluoromethylornithine, an inhibitor of ornithine decar
17 f cationic amino acid transport, or by alpha-difluoromethylornithine, an ornithine decarboxylase inhi
19 ine was inhibited by the ODC inhibitor alpha-difluoromethylornithine, and L-proline generation was bl
24 We studied effects of the combination of difluoromethylornithine (DFMO) and sulindac on biomarker
26 toma (NB) cells with the ODC inhibitor alpha-difluoromethylornithine (DFMO) depleted polyamine pools
27 ibition of polyamine biosynthesis with alpha-difluoromethylornithine (DFMO) has been shown to inhibit
28 Depletion of cellular polyamines by DL-alpha-difluoromethylornithine (DFMO) induced levels of JunD mR
32 sms underlying the chemopreventive effect of difluoromethylornithine (DFMO) on the development of mam
33 eatment with the Odc suicide inhibitor alpha-difluoromethylornithine (DFMO) or Odc heterozygosity mar
34 We found that the inhibition of ODC by alpha-difluoromethylornithine (DFMO) resulted in a approximate
35 ty by RS1-Reg mutants and the ODC1 inhibitor difluoromethylornithine (DFMO) was measured in the absen
36 tion of the NO donor agents as well as alpha-difluoromethylornithine (DFMO), a known ODC inhibitor, w
37 of ODC/Ras double transgenic mice with alpha-difluoromethylornithine (DFMO), a specific inhibitor of
39 etermine the chemopreventive effect of alpha-difluoromethylornithine (DFMO), an enzyme-activated irre
40 by zinc deficiency can be inhibited by alpha-difluoromethylornithine (DFMO), an enzyme-activated, irr
41 amine levels in COS-7 cells induced by alpha-difluoromethylornithine (DFMO), an inhibitor of ornithin
42 cultured in the presence or absence of alpha-difluoromethylornithine (DFMO), an inhibitor of the poly
47 thout the ornithine decarboxylase inhibitor, difluoromethylornithine (DFMO), and induced to undergo a
48 lls were exposed to the specific ODC blocker difluoromethylornithine (DFMO), and ODC activity, intrac
49 the ornithine decarboxylase (ODC) inhibitor difluoromethylornithine (DFMO), beginning at the time th
50 N1,N11-diethylnorspermine (DENSPM) or alpha-difluoromethylornithine (DFMO), have synergistic effects
54 on with the polyamine biosynthesis inhibitor difluoromethylornithine (DFMO), provides a method to tar
55 A specific inhibitor of the transgene, alpha-difluoromethylornithine (DFMO), reversibly blocked the a
61 ration of the suicide inhibitor of ODC alpha-difluoromethylornithine (DFMO, 0.5% w/v) in the drinking
62 f two molecules that alter polyamine levels: difluoromethylornithine (DFMO; also called eflornithine)
63 orrelated in diabetic and control rats given difluoromethylornithine (DFMO; Marion Merrell Dow, Cinci
64 nhibiting ornithine decarboxylase with alpha-difluoromethylornithine dramatically enhanced the cytopl
65 atment with the biosynthesis inhibitor alpha-difluoromethylornithine during tetracycline removal inte
66 and the pharmacological agents piroxicam and difluoromethylornithine each reduced intestinal adenoma
69 on to that observed for putrescine and alpha-difluoromethylornithine in previous T. brucei ODC struct
70 ing ornithine decarboxylase (ODC) with alpha-difluoromethylornithine increased the levels of ATF-2 mR
71 Depletion of cellular polyamines by alpha-difluoromethylornithine induced levels of phosphorylated
73 , the polyamine biosynthesis inhibitor alpha-difluoromethylornithine inhibits the ability of MTAP-def
74 the ornithine decarboxylase inhibitor alpha-difluoromethylornithine or the S-adenosylmethionine deca
75 ed either apoptosis in the basal epithelium (difluoromethylornithine) or both apoptosis and vacuolati
76 ated with the polyamine synthesis inhibitor, difluoromethylornithine, or the K(ATP) channel inhibitor
79 stration of the suicidal ODC inhibitor alpha-difluoromethylornithine reduced UVB-induced BCCs in Ptch
80 interfering RNA or the competitive inhibitor difluoromethylornithine restored iNOS protein expression
81 he ornithine decarboxylase inhibitor L-alpha-difluoromethylornithine sensitized all of these leukemia
82 ptosis could be blocked by the ODC inhibitor difluoromethylornithine, the caspase inhibitors Z-VAD FM
83 m target of Akt, was also increased in alpha-difluoromethylornithine-treated cells, which was prevent
88 reatment with the ODC enzyme inhibitor alpha-difluoromethylornithine, which results in regression of
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