ライフサイエンスコーパス: nitroquinoline

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1 ed after cells were exposed to UV, X-rays, 4-nitroquinoline 1-oxide (4-NQO) and methyl methanesulfona

2 rpholinosydnonimine hydrochloride (SIN-1), 4-nitroquinoline 1-oxide (4-NQO) and tert-butylhydroperoxi

3 l carcinogenesis induced by the carcinogen 4-nitroquinoline 1-oxide (4-NQO) in a mouse model of human

4 al agents methyl methanesulfonate (MMS) or 4-nitroquinoline 1-oxide (4-NQO) produces a 4- to 10-fold

5 We have developed a novel 4-nitroquinoline 1-oxide (4-NQO)-induced mouse model of es

6 Chronic exposure to the carcinogen 4-nitroquinoline 1-oxide (4-NQO, a UV-mimetic compound) in

7 al carcinogenesis in transgenic mice using 4-nitroquinoline 1-oxide (4NQO) resulted in more extensive

8 tract carcinogenesis upon initiation with 4-nitroquinoline 1-oxide (4NQO).

9 revisiae after exposure to the UV mimetic, 4-nitroquinoline 1-oxide (4NQO).

10 4-Nitroquinoline 1-oxide (NQO) is a reactive electrophile

11 variation in response to both drugs (e.g., 4-nitroquinoline 1-oxide [4NQO]) and different carbon sour

12 increased sensitivity to camptothecin and 4-nitroquinoline 1-oxide similar to that in cells lacking

13 t cell line is 6-18-fold more sensitive to 4-nitroquinoline 1-oxide than SV40-transformed normal cell

14 The DNA-damaging agent 4-nitroquinoline 1-oxide was applied to NIH-3T3 cells over

15 inal pigment epithelial (ARPE)-19 cells to 4-nitroquinoline 1-oxide, a UV-mimetic and adduct-forming

16 -damaging agents including UV irradiation, 4-nitroquinoline 1-oxide, camptothecin, etoposide, hydroxy

17 We showed that after 4-nitroquinoline 1-oxide-induced DNA damage, IGF-I induced

18 ifically in response to UV irradiation and 4-nitroquinoline 1-oxide.

19 th oral squamous carcinogenesis induced by 4-nitroquinoline 1-oxide.

20 ic metabolism of a simple nitroaryl probe, 6-nitroquinoline (1).

21 irradiation and by the UV-mimetic compound 4-nitroquinoline-1-oxide (4-NQO) and that a functional RSP

22 ells to both chronic and acute exposure to 4-nitroquinoline-1-oxide (4-NQO) but not to UV or cisplati

23 The UV radiation-mimetic chemical 4-nitroquinoline-1-oxide (4-NQO) is thought to induce squa

24 ensitivity of UV61 cells to the carcinogen 4-nitroquinoline-1-oxide (4-NQO), which introduces bulky D

25 er treatment with the chemical carcinogen, 4-nitroquinoline-1-oxide (4-NQO).

26 ellular stress that introduces DNA damage: 4-nitroquinoline-1-oxide (4NQO), gamma-irradiation, or UV-

27 teristics of WS cells: hypersensitivity to 4-nitroquinoline-1-oxide (4NQO), reduced replicative poten

28 ious reports have shown that two thirds of 4-nitroquinoline-1-oxide (4NQO)-induced murine oral squamo

29 s are characteristically hypersensitive to 4-nitroquinoline-1-oxide (4NQO).

30 ut independently of DNA lesions induced by 4-nitroquinoline-1-oxide in Saccharomyces cerevisiae.

31 th DNA-damaging agents such as UV light or 4-nitroquinoline-1-oxide induces polyubiquitylation of the

32 ]pyrene diol epoxide, gamma-radiation, and 4-nitroquinoline-1-oxide sensitivity, respectively.

33 synthesis, 16 acapsular mutants induced by 4-nitroquinoline-1-oxide were obtained.

34 sitized P. aeruginosa to nitrofurazone and 4-nitroquinoline-1-oxide, consistent with a role for DinB(

35 of RpoS also increases cell sensitivity to 4-nitroquinoline-1-oxide, indicating that RpoS affects the

36 egraded at the active genes in response to 4-nitroquinoline-1-oxide-induced DNA damage in Saccharomyc

37 5-Nitroisoquinoline and 6-nitroquinoline condensed with ethyl isocyanoacetate in t

38 ection from UV-mimetic-induced DNA damage, 4-nitroquinoline N-oxide (4-NQO) was used.

39 o the drugs cycloheximide, oligomycin, and 4-nitroquinoline N-oxide (4-NQO).

40 The carcinogenic compounds 4-nitroquinoline N-oxide, ethyl methanesulfonate, diethyls

41 nthracene (2-AA), an indirect mutagen, and 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward

42 nthracene (2-AA), an indirect mutagen, and 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward

43 nthracene (2-AA), an indirect mutagen; and 4-nitroquinoline-N-oxide (4-NQO), a direct mutagen toward

44 decreased resistance to hydrogen peroxide, 4-nitroquinoline-N-oxide (4-NQO), benomyl, and cadmium chl

45 uced proliferative survival in response to 4-nitroquinoline-N-oxide (4NQO) and 8-methoxypsoralen (8MO

46 er hypersensitivity to UV radiation and to 4-nitroquinoline-N-oxide and significantly reduce Pol V-de

47 e resistance to 3-amino-1,2,4-triazole and 4-nitroquinoline-N-oxide but only if the ATR1 gene is inta

48 ve compounds inhibited the mutagenicity of 4-nitroquinoline-N-oxide, a direct mutagen, and benzo[a]py

49 raction following DNA damage introduced by 4-nitroquinoline-N-oxide, camptothecin or partial inactiva

50 bitor reveromycin A and DNA damaging agent 4-nitroquinoline-N-oxide.

51 ffect on antiproliferative activity of the 5-nitroquinoline SN24349 in both genetic backgrounds after

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