ライフサイエンスコーパス: nitroquinoline

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 ell carcinoma (OSCC) induced by carcinogen 4-nitroquinoline 1-oxide (4NQO), mimicking molecular and h

9 induced the mice to develop OSCC by using 4-nitroquinoline 1-oxide (4NQO).

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

11 -type mice were exposed to the carcinogen, 4-nitroquinoline 1-oxide (4NQO).

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

13 4-Nitroquinoline 1-oxide (NQO) is a reactive electrophile

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

15 n contrast, although ultraviolet light and 4-nitroquinoline 1-oxide induce ribosome stalling by damag

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

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

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

19 ns in both the xenograft and a carcinogen (4-nitroquinoline 1-oxide)-induced oral cancer mouse models

20 icrobiota in an induced HNSCC mouse model (4-Nitroquinoline 1-oxide, 4NQO) and reconstitution of tumo

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

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

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

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

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

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

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

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

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

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

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

32 This model employs 4-nitroquinoline-1-oxide (4NQO) as an RS-inducing agent.

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

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

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

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

37 On treatment with the carcinogen 4-nitroquinoline-1-oxide Casp8(-/-) mice showed increased

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

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

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

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

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

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

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

45 5-Nitroisoquinoline and 6-nitroquinoline condensed with ethyl isocyanoacetate in t

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

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

48 type and GPR68(-/-) mice were treated with 4-Nitroquinoline N-oxide (4NQO) in drinking water for 11-1

49 99A cells were cultured in the presence of 4-nitroquinoline N-oxide (4NQO), N-nitroso-N-methylurea (M

50 with BK3C231 before exposure to carcinogen 4-nitroquinoline N-oxide (4NQO).

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

52 To establish whether 4-nitroquinoline N-oxide-induced carcinogenesis mirrors th

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

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

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

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

57 In C57BL/6 mice given 4-nitroquinoline-N-oxide (4-NQO), there was increased MPO

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

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

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

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

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

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

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