ライフサイエンスコーパス: nitrosoguanidine

1 1-type methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.

2 to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.

3 eeks after treatment with 1-methyl-3-nitro-1-nitrosoguanidine.

4 c cancer model induced by 1-methyl-3-nitro-1-nitrosoguanidine.

5 agent and PARP activator N-methyl-N'-nitro-N-nitrosoguanidine.

6 sis after treatment with N-methyl-N'-nitro-N-nitrosoguanidine.

7 the DNA-alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine.

8 croM BG and 40 microg/ml N-methyl-N'-nitro-N-nitrosoguanidine.

9 nous AGT from killing by N-methyl-N'-nitro-N-nitrosoguanidine.

10 ith the chemical mutagen N-methyl-N'-nitro-N-nitrosoguanidine.

11 y of the mutagenic agent N-methyl-N'-nitro-N-nitrosoguanidine.

12 the DNA alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, a potent PARP-1 activator, to study PA

13 to 6-thioguanine, cisplatin, and N-methyl-N'-nitrosoguanidine, an increase in the rate of generation

14 with resistance to both N-methyl-N'-nitro-N-nitrosoguanidine and BG.

15 otection from killing by N-methyl-N'-nitro-N-nitrosoguanidine and caused a reduction in m(6)G-induced

16 rotype 1, were isolated after treatment with nitrosoguanidine and enrichment with penicillin and D-cy

17 cells were 2-fold resistant to methyl-nitro-nitrosoguanidine and had a 65-fold elevated mutation rat

18 cytotoxicity induced by N-methyl-N'-nitro-N-nitrosoguanidine and menadione after benzamide withdrawa

19 , N-methyl-N-nitrosourea, N-methyl-N'nitro-N-nitrosoguanidine and methyl methanesulfonate and longer

20 nd mutagenic activity of N-methyl-N'-nitro-N-nitrosoguanidine and was more effective in preventing mu

21 the best protection from N-methyl-N'-nitro-N-nitrosoguanidine and, thus, is a promising gene therapy

22 -breaking agents (such asN-methyl-N'-nitro-N-nitrosoguanidine) and, subsequently, using biotinylated

23 on, an alkylating agent (N-methyl-N'-nitro-N-nitrosoguanidine), and gamma radiation, none of which re

24 by the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine, and thereby enables Escherichia coli t

25 ion was mutagenized with N-methyl-N'-nitro-N-nitrosoguanidine, and three mutants that had higher leve

26 to the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, both phenotypes consistent with mismat

27 the DNA-damaging agent, N-methyl-N'-nitro-N-nitrosoguanidine, despite the fact that no PARP protein

28 reas DNA damage by UV or N-methyl-N'-nitro-N-nitrosoguanidine did not result in enhanced mutagenesis.

29 N-Methyl-N'-nitro-N-nitrosoguanidine, etoposide, and bleomycin also induced

30 ls; UV light exposure or N-methyl-N'-nitro-N-nitrosoguanidine exposure increases mutant frequency sim

31 N-methyl-N'-nitro-N-nitrosoguanidine, H2O2, and N-methyl-d-aspartate induce

32 affect, the toxicity of N-methyl-N'-nitro-N-nitrosoguanidine in an alklyltransferase-proficient and

33 Two treatments with 1-methyl-3-nitro-1-nitrosoguanidine in the REL606 lineage produced at least

34 adiation and an alkylating agent N-methyl-N'-nitrosoguanidine in these immortalized or transformed ce

35 and mutagenic effects of N-methyl-N'-nitro-N-nitrosoguanidine, increasing the D37 over 4-fold and red

36 a recent screen of NTG (N-methyl-N'-nitro-N-nitrosoguanidine)-induced whi strains, was defined by tw

37 h TPA partially inhibited UV- or N-methyl-N'-nitrosoguanidine-induced JNK activity.

38 Nitrosoguanidine-induced mutants of strain BD413 were is

39 ucts, we have shown that N-methyl-N'-nitro-N-nitrosoguanidine-induced transcriptional activation of t

40 the ovine pathogen Chlamydia abortus and its nitrosoguanidine-induced, temperature-sensitive, virulen

41 nk of cells defective for 1-methyl-3-nitro-1-nitrosoguanidine-inducible genes revealed that defects i

42 al DNA alkylating agent N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) also triggers up-regulation and

43 of DNA-methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and antimetabolite 6-thioguanine

44 methanesulfonate (MMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and mechlorethamine HCl (HN2), o

45 thylating agents such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and methyl methane sulfonate (MM

46 by the DNA damaging agent N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and rescues cells from G1 arrest

47 lkylating agents such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) are known to covalently link alk

48 er cells were exposed to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) at 10(-5) mol/L for 48 hours, th

49 r alkylation damage from N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) by activating ATR (ataxia telang

50 such as the nitrosourea N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) elicit a G2/M checkpoint respons

51 hia coli from killing by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) even in the presence of BG and t

52 to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) exhibited a microsatellite insta

53 osing cells to 50 microM N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for increasing lengths of time a

54 the DNA-alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces expression of the endoge

55 N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) is a direct-acting monofunctiona

56 N-Methyl-N'-nitro-N'-nitrosoguanidine (MNNG) is a DNA-methylating agent, and

57 lkylating agents such as N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) on DNA.

58 by the genotoxic agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or 3-morpholinosydnonimine (SIN-

59 reviously initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resulted in a concentration depe

60 ), is enhanced following N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) treatment.

61 f the methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) when expressed in Escherichia co

62 the cytotoxic action of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) while abrogation of such repair

63 yl methane sulfonate and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)) was dependent on H2AX dosage, a

64 ) confers sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), a functional analogue of temozo

65 lating agents, including N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), a potent carcinogen.

66 th the alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and the AGT inhibitor, O6-benzy

67 exposed to the genotoxin N-methyl-N-nitro-N-nitrosoguanidine (MNNG), both cell lines underwent cytol

68 ic cells when exposed to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but normal human oral keratinoc

69 Following exposure to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), Msh2 deficient mice show a redu

70 genic and cytotoxic drug N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), robustly activate the DNA damag

71 zo(a)pyrene diol epoxide, N-methyl-N-nitro-N-nitrosoguanidine (MNNG), t-butyl hydrogen peroxide, and

72 R was also challenged by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), which generates O(6)-methylguan

73 ond to DNA alkylation by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), which triggers the MMR system.

74 ylating agents including N-methyl-N'-nitro-N-nitrosoguanidine (MNNG),which is known to cause colon ca

75 widely used laboratory strain that carries a nitrosoguanidine (MNNG)-induced mutation enabling it to

76 he fine structure map of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced mutations was determined

77 xide (H(2)O(2)), but not N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced PARP-1 hyperactivation a

78 is approach by measuring N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced point mutations in a 121

79 cy, either background or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced, in NHOK expressing the

80 ultraviolet B (UVB)- and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-treated fibroblasts showed incre

81 apoptosis in response to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

82 he DNA methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

83 th the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

84 he DNA alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

85 astoid line treated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG).

86 om the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG); (b) repair methylated DNA in vi

87 potent than cisplatin and N-methyl-N'-nitro-nitrosoguanidine (MNNG, a common DNA-alkylating chemothe

88 ate-containing media were isolated following nitrosoguanidine mutagenesis.

89 cts in arsenate resistance were generated by nitrosoguanidine mutagenesis.

90 were identified following hydroxylamine and nitrosoguanidine mutagenesis.

91 This strain was initially isolated following nitrosoguanidine mutagenesis.

92 We selected N-methyl-N'-nitro-N-nitrosoguanidine mutants in the cloned 4A' gene that no

93 and after treatment with N-methyl-N'-nitro-N-nitrosoguanidine (NTG) and 5-azacytidine (5AZ).

94 ee previously described N'-methyl-N'-nitro-N-nitrosoguanidine (NTG) mutants were mapped and cloned by

95 otoxic concentrations of N-methyl-N'-nitro-N-nitrosoguanidine or 3-morpholinosydnonimine to induce DN

96 -methyl-N-nitrosourea or N-methyl-N'-nitro-N-nitrosoguanidine results in p53 phosphorylation on serin

97 PARP-1 activating agent, N-methyl-N'-nitro-N-nitrosoguanidine, suggesting reduced capacity for PARP-1

98 s were more sensitive to N-methyl-N'-nitro-N-nitrosoguanidine than the 16.3 cells.

99 restored sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine treatment and mismatch repair activity.

100 tability, sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine treatment, and mismatch repair activity

101 6) and was increased more than 1,000-fold by nitrosoguanidine treatment.

102 -dependent fashion after N-methyl-N'-nitro-N-nitrosoguanidine treatment.

103 stabilize p53 following N-methyl-N'-nitro-N-nitrosoguanidine treatment.

104 hylmethane sulfonate and N-methyl-N'-nitro-N-nitrosoguanidine, which cause phosphorylation of p53 at

105 th the UVM-inducing agent 1-methyl-3-nitro-1-nitrosoguanidine, with subsequent transfection of M13 vi