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1 reated with a selective inhibitor of NQO(1), dicumarol.
2 enten kinetics and was markedly inhibited by dicumarol, a competitive inhibitor of naphthoquinone oxi
3                                              Dicumarol also inhibited cell growth, plating efficiency
4                                 In addition, dicumarol, an inhibitor of the phase II detoxifying enzy
5      The enzymatic activity was inhibited by dicumarol, anti-coagulant drug, with IC50 of 4 microm.
6                                              Dicumarol decreased clonogenic survival equally in both
7                                              Dicumarol decreased clonogenic survival in the transform
8                                     Although dicumarol has been used as an inhibitor of the two-elect
9 vity is insensitive to rotenone, flavone, or dicumarol; however, it was inhibited by diphenyl iodoniu
10                                              Dicumarol increased intracellular production of O(2)(.-)
11 atalase with adenoviral vectors reversed the dicumarol-induced cytotoxicity and reversed fluorescence
12  increased susceptibility of cancer cells to dicumarol-induced cytotoxicity.
13 susceptibility of pancreatic cancer cells to dicumarol-induced metabolic oxidative stress.
14 ibitable NAD(P)H:menadione oxidoreductase or dicumarol-inhibitable NAD(P)H:dichlorophenolindophenol r
15 ified DT-diaphorase can be assayed as either dicumarol-inhibitable NAD(P)H:menadione oxidoreductase o
16  When DT-diaphorase activity was measured as dicumarol-inhibitable NADPH:dichlorophenolindophenol red
17 bstances of widely different molecular size: dicumarol, insulin and plasmid DNA.
18                                              Dicumarol is a naturally occurring anticoagulant derived
19 ctase NAD(P)H:quinone oxidoreductase (NQO1), dicumarol is also thought to affect quinone-mediated ele
20 H, or NMNH; (ii) is very weakly inhibited by dicumarol or Cibacron blue; (iii) is very potently inhib
21           Moreover, using inhibitors of GST (dicumarol) or MRP1 (sulfinpyrazone), it was shown that i
22 inone oxidoreductase enzymatic activity with dicumarol prior to quinone treatment resulted in increas
23 using mitomycin (trial 1) and mitomycin with dicumarol (trial 2) as an adjunct to radiation therapy i
24  or without mitomycin (trial 1) or mitomycin/dicumarol (trial 2).
25                                              Dicumarol with the mitochondrial electron transport chai
26                                              Dicumarol, with the addition of mitochondrial electron t

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