ライフサイエンスコーパス: methylating agent

1 intermediate (dpms)Pt(IV)Me(OH)2 (8), a good methylating agent.

2 c route to an extremely potent electrophilic methylating agent.

3 ing the cell against killing by the Sn1-type methylating agent.

4 e (m7dG) is the predominant lesion formed by methylating agents.

5 ious organisms in the presence of S(N)2 type methylating agents.

6 produced by various endogenous and exogenous methylating agents.

7 ajor cytotoxic lesion formed in DNA by S(N)2 methylating agents.

8 calize with hRad9 foci in cells treated with methylating agents.

9 dinates the resistance response to genotoxic methylating agents.

10 and tetramethylammonium hydroxide (TMAH) as methylating agents.

11 nt and to resistance to chemotherapeutic DNA-methylating agents.

12 system in the cytotoxic response to Sn1-type methylating agents.

13 to sensitize tumor cells to chemotherapeutic methylating agents.

14 s and induced mutagenesis, and resistance to methylating agents.

15 atch repair, which renders them resistant to methylating agents.

16 cal explanation for cellular cytotoxicity of methylating agents.

17 coli alkB mutants are very sensitive to DNA methylating agents.

18 r of DNA damage induced by cross-linking and methylating agents.

19 ystem, which may explain their resistance to methylating agents.

20 r resistance to the cytotoxic effects of DNA-methylating agents.

21 undergoes chemical conversion to the active methylating agent 5-(3-methyltriazen-1yl)imidazole-4-car

22 enhanced the tumorigenic activity of a model methylating agent, acetoxymethylmethylnitrosamine (AMMN)

23 higher cytotoxicity than cells treated with methylating agent alone.

24 we report that TrmFO carries an active tRNA-methylating agent and characterize it as an original enz

25 has been accomplished using methanol as the methylating agent and the hydrogen-borrowing method.

26 ine is a minor lesion that is induced by DNA-methylating agents and for which no repair process has b

27 deficient cells after treatment with various methylating agents and other base analogues has been wel

28 epair system in the cytotoxic effects of DNA-methylating agents and suggest that recognition of 1,2-i

29 N'-nitro-N'-nitrosoguanidine (MNNG) is a DNA-methylating agent, and deficiency in mismatch repair (MM

30 Methylating agents are widespread environmental carcinog

31 protein protects against the cytotoxicity of methylating agents by repair of the DNA lesions 1-methyl

32 richia coli to respond to small doses of DNA-methylating agents by upregulating the expression of fou

33 Treatment with hypo-methylating agents can lead to expression of these silen

34 nine (3MeA), can be induced by environmental methylating agents, chemotherapeutics, and natural cellu

35 are induced to a much lower level by the SN2 methylating agent dimethyl sulfate and repaired much fas

36 ld-type APC gene was more sensitive to a DNA-methylating agent due to decreased DNA repair by long pa

37 enic and is commonly found in DNA exposed to methylating agents, even physiological ones (e.g. S-aden

38 Methylating agents generate cytotoxic and mutagenic DNA

39 The addition of the methylating agent had no effect on Gram-positive bacteri

40 se (AGT), which repairs DNA damage caused by methylating agents, has not been demonstrated.

41 activity of beta-pol is required to reverse methylating agent hypersensitivity in beta-pol null cell

42 wn that mouse fibroblasts treated with a DNA methylating agent in combination with a PARP inhibitor e

43 SAMe also acts as the main methylating agent in the liver.

44 ects in MMR appear particularly resistant to methylating agents in a manner that overrides dependence

45 c, can influence the tumorigenic activity of methylating agents in two ways.

46 Following treatment with DNA-methylating agents, increased persistence of 7-meG was f

47 y relevant doses, chemotherapeutic S(N)1 DNA methylating agents induce an ATR-mediated checkpoint res

48 Thus, in MMR deficient tissues, methylating agents induce point mutations in cells with

49 tizes glioblastoma cells to chemotherapeutic methylating agent-induced cytotoxicity.

50 mined the contribution of the Akt pathway to methylating agent-induced G2 arrest and toxicity.

51 mediate, and documents latency shortening by methylating agent-induced mutation of K-ras.

52 ich is produced in DNA following exposure to methylating agents, instructs human RNA polymerase II to

53 Cytotoxicity of methylating agents is caused mostly by methylation of th

54 e and in mice pretreated for 7 days with the methylating agent methionine (750 mg/kg i.p.).

55 e fibroblasts is hypersensitivity to the DNA-methylating agent methyl methanesulfonate.

56 rats born to dams administered with the DNA-methylating agent methylazoxymethanol acetate (MAM) at g

57 mal growth conditions and in response to the methylating-agent methylmethane sulfonate (MMS) and ioni

58 hen clone 5 cells were exposed to the simple methylating agent methylnitrosourea (MNU) without previo

59 or 16 h and is also seen with the S(N)1-type methylating agent methylnitrosourea.

60 in erb-B-3 transgenic mice treated with the methylating agent, methylnitrosourea [MNU].

61 s of radA were modestly sensitive to the DNA-methylating agent MMS and to the DNA strand breakage age

62 xic and not mutagenic and was induced by SN2 methylating agents, MMS, DMS, and MeI but not by SN1 age

63 e deficient (MGMT(-)), were treated with the methylating agent MNNG to create a level of O(6)-methylg

64 ns in animal models of cancer induced by the methylating agent MNU.

65 ecreased apoptosis upon the treatment of DNA-methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (

66 damage signaling pathways induced by the DNA methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (

67 arrest and apoptosis upon treatment with the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (

68 bility (CIN), whereas cells resistant to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (

69 owing: (a) protect Escherichia coli from the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (

70 protein repairs the DNA damage caused by the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine,

71 ient Escherichia coli with resistance to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.

72 rad52Delta cells to the prototypic Sn1-type methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.

73 are cross-resistant to 6-thioguanine and the methylating agent N-methyl-N-nitrosourea (MNU).

74 ATR activation induced by the DNA methylating agent N-methyl-N-nitrosourea was also shown

75 the cytotoxic and mutagenic activity of the methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine

76 petent wild-type cells by treatment with the methylating agent, N-methyl-N-nitrosourea.

77 more susceptible to the toxic effects of the methylating agents, N-methyl-N-nitrosourea, N-methyl-N'n

78 ency does not affect tolerance of flies to a methylating agent nor does it affect resistance to gamma

79 orms in human genomic DNA upon reaction with methylating agents of dietary, environmental, or endogen

80 ct DNA damage from an epoxide metabolite and methylating agents on a reaction time scale of minutes.

81 e damage, and to cell killing induced by two methylating agents, one of which produces almost exclusi

82 Thus, methylating agents potentiate lymphomagenesis of LMO1, i

83 ce are hypersensitive to mono-functional DNA-methylating agents, resulting in increases in chromosoma

84 iotic carcinogens but also by the endogenous methylating agent S-adenosylmethionine.

85 Inspiration from Nature's methylating agent, S-adenosylmethionine (SAM), allowed f

86 A alkyltransferase (AGT) levels is to modify methylating agent scheduling.

87 ta, are hypersensitive to monofunctional DNA methylating agents such as methyl methanesulfonate (MMS)

88 Methylating agents such as N-methyl-N'-nitro-N-nitrosogu

89 sensitization of gliomas to chemotherapeutic methylating agents such as temozolomide.

90 and nitrosourea drugs such as carmustine and methylating agents such as temozolomide.

91 SN1 DNA methylating agents such as the nitrosourea N-methyl-N'-n

92 We compared resistance to the methylating agent temozolomide (TMZ) and to the chloroet

93 glioma cells exposed to the chemotherapeutic methylating agent temozolomide (TMZ) but not in paired c

94 ure of Lgr5-CreERT2;Msh2(flox/-) mice to the methylating agent temozolomide caused MSH2-deficient int

95 recipients were observed or treated with the methylating agent, temozolomide (TMZ).

96 mbination and by the chemical synthesis of a methylating agent that almost exclusively produces 3-met

97 o potentiate by 5-fold the toxicity of a DNA methylating agent that creates abasic sites.

98 Temozolomide (TMZ) is a DNA-methylating agent that has recently been introduced into

99 number of DNA-damaging compounds, including methylating agents that produce O(6)-methylguanine (O(6)

100 Methylating agent tolerance was evident by the competiti

101 sed to examine the effects of MMR status and methylating agent treatment on cellular expression of DN

102 Although human cells exposed to DNA-methylating agents undergo mismatch repair (MMR)-depende

103 ve of lesions generated by oxygen damage and methylating agents, were incorporated into the DNA stran

104 relatively minor DNA lesion produced by most methylating agents (which form mainly 7-methylguanine),

105 rad52Delta cells to treatment with Sn1-type methylating agents, which produce cytotoxic O(6)-methylg