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1 ing as a low-cost but efficient reducing and methylating agent.
2 P in sensitizing cultured cells toward a DNA methylating agent.
3 intermediate (dpms)Pt(IV)Me(OH)2 (8), a good methylating agent.
4 c route to an extremely potent electrophilic methylating agent.
5 ing the cell against killing by the Sn1-type methylating agent.
6  and tetramethylammonium hydroxide (TMAH) as methylating agents.
7 ystem, which may explain their resistance to methylating agents.
8 r resistance to the cytotoxic effects of DNA-methylating agents.
9 system in the cytotoxic response to Sn1-type methylating agents.
10 ge that can arise, in part, from exposure to methylating agents.
11 ike oxonium ions with methanol as the active methylating agents.
12 (ko) cells were only resistant to S(N)1-type methylating agents.
13 r of DNA damage induced by cross-linking and methylating agents.
14 e (m7dG) is the predominant lesion formed by methylating agents.
15 ious organisms in the presence of S(N)2 type methylating agents.
16 produced by various endogenous and exogenous methylating agents.
17 ajor cytotoxic lesion formed in DNA by S(N)2 methylating agents.
18 calize with hRad9 foci in cells treated with methylating agents.
19 dinates the resistance response to genotoxic methylating agents.
20 nt and to resistance to chemotherapeutic DNA-methylating agents.
21 to sensitize tumor cells to chemotherapeutic methylating agents.
22 s and induced mutagenesis, and resistance to methylating agents.
23 atch repair, which renders them resistant to methylating agents.
24 cal explanation for cellular cytotoxicity of methylating agents.
25  coli alkB mutants are very sensitive to DNA methylating agents.
26  methylation was investigated using the hypo-methylating agent 5'-aza-2'-deoxycytidine (5-aza-dC) in
27  undergoes chemical conversion to the active methylating agent 5-(3-methyltriazen-1yl)imidazole-4-car
28 enhanced the tumorigenic activity of a model methylating agent, acetoxymethylmethylnitrosamine (AMMN)
29  higher cytotoxicity than cells treated with methylating agent alone.
30  we report that TrmFO carries an active tRNA-methylating agent and characterize it as an original enz
31  has been accomplished using methanol as the methylating agent and the hydrogen-borrowing method.
32 ine is a minor lesion that is induced by DNA-methylating agents and for which no repair process has b
33 deficient cells after treatment with various methylating agents and other base analogues has been wel
34 epair system in the cytotoxic effects of DNA-methylating agents and suggest that recognition of 1,2-i
35 N'-nitro-N'-nitrosoguanidine (MNNG) is a DNA-methylating agent, and deficiency in mismatch repair (MM
36 guanosine (N7-MedG), a marker of exposure to methylating agents, and other markers of DNA damage and
37                                              Methylating agents are widespread environmental carcinog
38 protein protects against the cytotoxicity of methylating agents by repair of the DNA lesions 1-methyl
39 richia coli to respond to small doses of DNA-methylating agents by upregulating the expression of fou
40  cell response to the cytotoxic effects of a methylating agent can determine the effects of VUS in MM
41                          Treatment with hypo-methylating agents can lead to expression of these silen
42 that undergo death following exposure to the methylating agent; cells that escaped its toxicity were
43 nine (3MeA), can be induced by environmental methylating agents, chemotherapeutics, and natural cellu
44 are induced to a much lower level by the SN2 methylating agent dimethyl sulfate and repaired much fas
45 ld-type APC gene was more sensitive to a DNA-methylating agent due to decreased DNA repair by long pa
46 enic and is commonly found in DNA exposed to methylating agents, even physiological ones (e.g. S-aden
47                       Male mice exposed to a methylating agent exhibited a reduced number of PR cell
48 mmonium iodide (PhMe(3)NI) as an alternative methylating agent for introducing a CH(3) group in alpha
49                                              Methylating agents generate cytotoxic and mutagenic DNA
50                          The addition of the methylating agent had no effect on Gram-positive bacteri
51 se (AGT), which repairs DNA damage caused by methylating agents, has not been demonstrated.
52  activity of beta-pol is required to reverse methylating agent hypersensitivity in beta-pol null cell
53 wn that mouse fibroblasts treated with a DNA methylating agent in combination with a PARP inhibitor e
54 f TEMPO-Me produces a powerful electrophilic methylating agent in situ.
55                   SAMe also acts as the main methylating agent in the liver.
56 ects in MMR appear particularly resistant to methylating agents in a manner that overrides dependence
57 c, can influence the tumorigenic activity of methylating agents in two ways.
58                 Following treatment with DNA-methylating agents, increased persistence of 7-meG was f
59 y relevant doses, chemotherapeutic S(N)1 DNA methylating agents induce an ATR-mediated checkpoint res
60              Thus, in MMR deficient tissues, methylating agents induce point mutations in cells with
61 tizes glioblastoma cells to chemotherapeutic methylating agent-induced cytotoxicity.
62 mined the contribution of the Akt pathway to methylating agent-induced G2 arrest and toxicity.
63 mediate, and documents latency shortening by methylating agent-induced mutation of K-ras.
64 ich is produced in DNA following exposure to methylating agents, instructs human RNA polymerase II to
65                              Cytotoxicity of methylating agents is caused mostly by methylation of th
66 e and in mice pretreated for 7 days with the methylating agent methionine (750 mg/kg i.p.).
67 e fibroblasts is hypersensitivity to the DNA-methylating agent methyl methanesulfonate.
68  rats born to dams administered with the DNA-methylating agent methylazoxymethanol acetate (MAM) at g
69 mal growth conditions and in response to the methylating-agent methylmethane sulfonate (MMS) and ioni
70 hen clone 5 cells were exposed to the simple methylating agent methylnitrosourea (MNU) without previo
71 or 16 h and is also seen with the S(N)1-type methylating agent methylnitrosourea.
72  in erb-B-3 transgenic mice treated with the methylating agent, methylnitrosourea [MNU].
73 s of radA were modestly sensitive to the DNA-methylating agent MMS and to the DNA strand breakage age
74 xic and not mutagenic and was induced by SN2 methylating agents, MMS, DMS, and MeI but not by SN1 age
75 e deficient (MGMT(-)), were treated with the methylating agent MNNG to create a level of O(6)-methylg
76 ns in animal models of cancer induced by the methylating agent MNU.
77 damage signaling pathways induced by the DNA methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (
78 ecreased apoptosis upon the treatment of DNA-methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (
79 arrest and apoptosis upon treatment with the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (
80 bility (CIN), whereas cells resistant to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (
81 owing: (a) protect Escherichia coli from the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine (
82 protein repairs the DNA damage caused by the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine,
83 ient Escherichia coli with resistance to the methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.
84  rad52Delta cells to the prototypic Sn1-type methylating agent N-methyl-N'-nitro-N-nitrosoguanidine.
85 are cross-resistant to 6-thioguanine and the methylating agent N-methyl-N-nitrosourea (MNU).
86            ATR activation induced by the DNA methylating agent N-methyl-N-nitrosourea was also shown
87  the cytotoxic and mutagenic activity of the methylating agent, N-methyl-N'-nitro-N-nitrosoguanidine
88 petent wild-type cells by treatment with the methylating agent, N-methyl-N-nitrosourea.
89 more susceptible to the toxic effects of the methylating agents, N-methyl-N-nitrosourea, N-methyl-N'n
90 ency does not affect tolerance of flies to a methylating agent nor does it affect resistance to gamma
91 orms in human genomic DNA upon reaction with methylating agents of dietary, environmental, or endogen
92 ct DNA damage from an epoxide metabolite and methylating agents on a reaction time scale of minutes.
93 e damage, and to cell killing induced by two methylating agents, one of which produces almost exclusi
94                                        Thus, methylating agents potentiate lymphomagenesis of LMO1, i
95 lso work in pathological cases, where common methylating agents provide N,N-dimethylated products in
96                     Compared to conventional methylating agents, quaternary ammonium salts have the a
97 ce are hypersensitive to mono-functional DNA-methylating agents, resulting in increases in chromosoma
98 iotic carcinogens but also by the endogenous methylating agent S-adenosylmethionine.
99 nucleic acids, amino acids and the universal methylating agent S-adenylsmethionine(1,2).
100                    Inspiration from Nature's methylating agent, S-adenosylmethionine (SAM), allowed f
101 A alkyltransferase (AGT) levels is to modify methylating agent scheduling.
102 ta, are hypersensitive to monofunctional DNA methylating agents such as methyl methanesulfonate (MMS)
103                                              Methylating agents such as N-methyl-N'-nitro-N-nitrosogu
104 sensitization of gliomas to chemotherapeutic methylating agents such as temozolomide.
105 and nitrosourea drugs such as carmustine and methylating agents such as temozolomide.
106                                      SN1 DNA methylating agents such as the nitrosourea N-methyl-N'-n
107                We compared resistance to the methylating agent temozolomide (TMZ) and to the chloroet
108 glioma cells exposed to the chemotherapeutic methylating agent temozolomide (TMZ) but not in paired c
109 ure of Lgr5-CreERT2;Msh2(flox/-) mice to the methylating agent temozolomide caused MSH2-deficient int
110 recipients were observed or treated with the methylating agent, temozolomide (TMZ).
111 mbination and by the chemical synthesis of a methylating agent that almost exclusively produces 3-met
112 o potentiate by 5-fold the toxicity of a DNA methylating agent that creates abasic sites.
113                  Temozolomide (TMZ) is a DNA-methylating agent that has recently been introduced into
114  number of DNA-damaging compounds, including methylating agents that produce O(6)-methylguanine (O(6)
115 l can be employed as a green and sustainable methylating agent to form C-C and C-N bonds via borrowin
116                                              Methylating agent tolerance was evident by the competiti
117 sed to examine the effects of MMR status and methylating agent treatment on cellular expression of DN
118 sing dimethyl sulfoxide as a nonconventional methylating agent under metal-free conditions was report
119          Although human cells exposed to DNA-methylating agents undergo mismatch repair (MMR)-depende
120 go death following DNA damage induction by a methylating agent, we were able to assess whether varian
121 MMR impacts ALKBH2 and/or ALKBH3 response to methylating agents, we generated cells deficient in ALKB
122 ve of lesions generated by oxygen damage and methylating agents, were incorporated into the DNA stran
123 nced resistance toward S(N)1- and S(N)2-type methylating agents, whereas MLH1(ko)ALKBH2(ko) cells wer
124 relatively minor DNA lesion produced by most methylating agents (which form mainly 7-methylguanine),
125  rad52Delta cells to treatment with Sn1-type methylating agents, which produce cytotoxic O(6)-methylg

 
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