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1 to the prototypic Sn1-type methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.
2 to the DNA-damaging agent and PARP activator N-methyl-N'-nitro-N-nitrosoguanidine.
3 ty to undergo apoptosis after treatment with N-methyl-N'-nitro-N-nitrosoguanidine.
4 d a minimal dose of the DNA-alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine.
5 treatment with 50 microM BG and 40 microg/ml N-methyl-N'-nitro-N-nitrosoguanidine.
6 WR109 lacking endogenous AGT from killing by N-methyl-N'-nitro-N-nitrosoguanidine.
7 ed after treatment with the chemical mutagen N-methyl-N'-nitro-N-nitrosoguanidine.
8 inst the cytotoxicity of the mutagenic agent N-methyl-N'-nitro-N-nitrosoguanidine.
9 oli with resistance to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.
12 exhibited similar protection from killing by N-methyl-N'-nitro-N-nitrosoguanidine and caused a reduct
13 eased sensitivity to cytotoxicity induced by N-methyl-N'-nitro-N-nitrosoguanidine and menadione after
14 t both the killing and mutagenic activity of N-methyl-N'-nitro-N-nitrosoguanidine and was more effect
15 lso offered E. coli the best protection from N-methyl-N'-nitro-N-nitrosoguanidine and, thus, is a pro
16 methylating agents, N-methyl-N-nitrosourea, N-methyl-N'nitro-N-nitrosoguanidine and methyl methanesu
17 sure to UV-C radiation, an alkylating agent (N-methyl-N'-nitro-N-nitrosoguanidine), and gamma radiati
18 e DNA damage caused by the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine, and thereby enable
19 bacA386::TnphoA fusion was mutagenized with N-methyl-N'-nitro-N-nitrosoguanidine, and three mutants
20 increased tolerance to the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine, both phenotypes co
21 owing treatment with the DNA-damaging agent, N-methyl-N'-nitro-N-nitrosoguanidine, despite the fact t
22 llite sequences, whereas DNA damage by UV or N-methyl-N'-nitro-N-nitrosoguanidine did not result in e
24 ogenic wild-type cells; UV light exposure or N-methyl-N'-nitro-N-nitrosoguanidine exposure increases
26 ncreased, or did not affect, the toxicity of N-methyl-N'-nitro-N-nitrosoguanidine in an alklyltransfe
27 both the cytotoxic and mutagenic effects of N-methyl-N'-nitro-N-nitrosoguanidine, increasing the D37
28 i loci identified in a recent screen of NTG (N-methyl-N'-nitro-N-nitrosoguanidine)-induced whi strain
29 tion mutation constructs, we have shown that N-methyl-N'-nitro-N-nitrosoguanidine-induced transcripti
31 that the monofunctional DNA alkylating agent N-methyl-N'-nitro-N- nitrosoguanidine (MNNG) also trigge
32 upon the treatment of DNA-methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and antimeta
33 ents, such as methyl methanesulfonate (MMS), N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and mechlore
37 eckpoint arrest after alkylation damage from N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) by activatin
38 A methylating agents such as the nitrosourea N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) elicit a G2/
39 A protected Escherichia coli from killing by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) even in the
40 eas cells resistant to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) exhibited a
41 s was induced by exposing cells to 50 microM N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) for increasi
42 tment of cells with the DNA-alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) induces expr
45 tivation was induced by the genotoxic agents N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) or 3-morphol
46 addition to cells previously initiated with N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) resulted in
47 precipitation (Co-IP), is enhanced following N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) treatment.
48 mutagenic activity of the methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) when express
49 ia coli dam cells to the cytotoxic action of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) while abroga
50 ylating agents (methyl methane sulfonate and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)) was depende
51 chromosome 10 (PTEN) confers sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), a functiona
52 roduced by many alkylating agents, including N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), a potent ca
53 coli resistant to both the alkylating agent, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), and the AGT
54 convert to tumorigenic cells when exposed to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), but normal
56 ts, such as the mutagenic and cytotoxic drug N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), robustly ac
58 how p21 levels respond to DNA alkylation by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), which trigg
59 r cell line with alkylating agents including N-methyl-N'-nitro-N-nitrosoguanidine (MNNG),which is kno
60 t this hypothesis, the fine structure map of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced muta
61 ogates hydrogen peroxide (H(2)O(2)), but not N-Methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced PARP
62 We have tested this approach by measuring N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced poin
63 The mutation frequency, either background or N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-induced, in
64 racts prepared from ultraviolet B (UVB)- and N-methyl-N'-nitro-N-nitrosoguanidine (MNNG)-treated fibr
70 Escherichia coli from the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG); (b) repair
71 cell death induced by the DNA damaging agent N-methyl-N-nitro-N-nitrosoguanidine (MNNG) and rescues c
72 ing p53) cells were exposed to the genotoxin N-methyl-N-nitro-N-nitrosoguanidine (MNNG), both cell li
73 ma-irradiation, benzo(a)pyrene diol epoxide, N-methyl-N-nitro-N-nitrosoguanidine (MNNG), t-butyl hydr
75 rbs1 alleles from three previously described N'-methyl-N'-nitro-N-nitrosoguanidine (NTG) mutants were
76 icient) backgrounds and after treatment with N-methyl-N'-nitro-N-nitrosoguanidine (NTG) and 5-azacyti
77 treated with the cytotoxic concentrations of N-methyl-N'-nitro-N-nitrosoguanidine or 3-morpholinosydn
78 )1 DNA methylators N-methyl-N-nitrosourea or N-methyl-N'-nitro-N-nitrosoguanidine results in p53 phos
79 re resistant to the PARP-1 activating agent, N-methyl-N'-nitro-N-nitrosoguanidine, suggesting reduced
80 the 16.3DeltaP cells were more sensitive to N-methyl-N'-nitro-N-nitrosoguanidine than the 16.3 cells
81 t the HPRT locus and restored sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine treatment and misma
82 red microsatellite stability, sensitivity to N-methyl-N'-nitro-N-nitrosoguanidine treatment, and mism
85 lkylating agents methylmethane sulfonate and N-methyl-N'-nitro-N-nitrosoguanidine, which cause phosph
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