ライフサイエンスコーパス: methylguanine

1 uenced by sequence context than that of O(6)-methylguanine.

2 atic side chains in a pocket that excludes 7-methylguanine.

3 repair kinetics of another Aag substrate, 7-methylguanine.

4 -methylhypoxanthine, 1-methylguanine, and N2-methylguanine.

5 tory, though less so than those containing 7-methylguanine.

6 role in the interaction with the flipped O6-methylguanine.

7 ontaining O6-benzylguanine and the other, O6-methylguanine.

8 stranded oligodeoxynucleotides containing O6-methylguanine.

9 4 cells can be decreased by treatment with 7-methylguanine.

10 phosphate, purine, xanthine, and 8-hydroxy-7-methylguanine.

11 cytotoxic of lesions generated by TMZ, O(6)-methylguanine.

12 ass spectrometry analysis of unrepaired O(6)-methylguanine.

13 f AlkA purine substrates (7-methyladenine, 7-methylguanine, 3-methyladenine, 3-methylguanine, purine,

14 examine the functions of this enzyme on O(6)-methylguanine (6mG) adducts in the four-stranded structu

15 transferase (AGT) show that it forms an O(6)-methylguanine (6mG)-specific complex on duplex DNA that

16 or methylazoxymethyl acetate (MAMAc), and 7-methylguanine (7-MeG) and O(6)-methylguanine (O(6)-MeG)

17 mals to release 3-methyladenine (3-meA) or 7-methylguanine (7-meG) from 3H-methylated calf thymus DNA

18 N-Methylpurines (NMPs), including N(7)-methylguanine (7MeG) and N(3)-methyladenine (3MeA), can

19 nd purine, whereas YjcD and YgfQ recognize 1-methylguanine, 8-azaguanine, 6-thioguanine, and 6-mercap

20 s explored using a model system comprising 9-methylguanine (9MG) and CH3NH2.

21 t, the pH-rate profile for the reaction of 7-methylguanine, a positively charged substrate, shows onl

22 pr-null mice correlated with reduced lung O6-methylguanine adduct levels, without decreases in NNK bi

23 otides containing a single well defined O(6)-methylguanine adduct were used to examine the extent of

24 This work shows a mechanism whereby O(6)-methylguanine adducts formed by temozolomide lead to inh

25 The ability of temozolomide to form O(6)-methylguanine adducts is important for inhibition of NF-

26 methyl sulfate-induced 3-methyladenine and 7-methylguanine adducts were measured at nucleotide resolu

27 causes cellular cytotoxicity by forming O(6)-methylguanine adducts.

28 alkyltransferase (AGT)-mediated repair of O6-methylguanine adducts.

29 itive to alkylating agents that result in O6-methylguanine adducts.

30 ntly, whereas 7,8-dihydro-8-oxoguanine, O(6)-methylguanine, adenine, and guanine were not.

31 ma and found that the enzyme releases both 7-methylguanine and 3-methyladenine from DNA.

32 ng in a fully functional protein for both O6-methylguanine and apurinic/apyrimidinic (AP) site repair

33 tized cells to the cytotoxic DNA lesion O(6)-methylguanine and caused a synthetic lethal interaction

34 is across SOS-independent lesions such as O6-methylguanine and DNA uracil is around 90%, very close t

35 -pyridyl)-1-butanone-induced short-term O(6)-methylguanine and long-term adenoma formation in the lun

36 gh a majority of the TMZ-induced lesions (N7-methylguanine and N3-methyladenine) are base excision re

37 for the repair of alkylated bases such as N7-methylguanine and N3-methyladenine.

38 itrosoguanidine (MNNG), which generates O(6)-methylguanine and O(4)-methylthymine recognized by MMR s

39 atinum(II), as well as base pairs between O6-methylguanine and thymine or cytosine, or between O4-met

40 gnize certain forms of DNA damage such as O6-methylguanine and UV photoproducts, and, therefore, mism

41 a C residue opposite an abasic site, an O(6)-methylguanine, and an 8-oxoguanine lesion, respectively.

42 ,N6-dimethyladenine, 1-methylhypoxanthine, 1-methylguanine, and N2-methylguanine.

43 ibited the formation of N7-methylguanine, O6-methylguanine, and O6-pyridyloxobutylguanine at a neighb

44 bind to oligodeoxynucleotides containing O6-methylguanine; and (d) react with the low molecular weig

45 sults identify N(2)-dGuo adducts bigger than methylguanine as a structural subclass of transcription-

46 tion is the result of MutS recognition of O6-methylguanine base pairs.

47 Slow excision rates for 7-methylguanine bases afforded the opportunity to study th

48 ro excision data indicates that removal of 7-methylguanine by the MPG protein is the rate-limiting st

49 ever, the persistence of a premutagenic O(6)-methylguanine can also be invoked.

50 most methylating agents (which form mainly 7-methylguanine), can specifically induce sister chromatid

51 ukaryotes is the addition of a 5'-terminal 7-methylguanine cap (m7GpppN) to nascent pre-mRNAs in the

52 rotein is capable of tightly binding to O(6)-methylguanine-containing DNA and disrupting its repair b

53 Demethylation of methylguanine could explain the presence in E. coli of t

54 LMO1 and MGMT, and thereby able to repair O6-methylguanine DNA adducts induced by MNU, would be prote

55 in family protein 1A (RASSF1A) (57%), and O6-methylguanine DNA methylatransferase (MGMT) (34%), and d

56 showed that, in addition to changes in O(6)-methylguanine DNA methyltransferase (MGMT) activity, sma

57 ve measurement of alkylation repair via O(6)-methylguanine DNA methyltransferase (MGMT) and base exci

58 The human DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) dealkylates m

59 l inactivation of the non-X-linked human O-6-methylguanine DNA methyltransferase (MGMT) gene has been

60 structure in the CpG island of the human O6-methylguanine DNA methyltransferase (MGMT) gene.

61 noic acid receptor-beta2 (RAR-beta2), and O6-methylguanine DNA methyltransferase (MGMT) genes were as

62 O6-methylguanine DNA methyltransferase (MGMT) is a DNA repa

63 the gene encoding the DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) might be redu

64 cells express extremely low levels of the O6-methylguanine DNA methyltransferase (MGMT) protein that

65 The DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) removes alkyl

66 O6-Methylguanine DNA methyltransferase (MGMT) removes alkyl

67 O6-Methylguanine DNA methyltransferase (MGMT) repairs the m

68 O(6)-methylguanine DNA methyltransferase (MGMT) suppresses mu

69 ed in this study to specifically target O(6)-methylguanine DNA methyltransferase (MGMT) to the mitoch

70 shown that modification of yd T cells with a methylguanine DNA methyltransferase (MGMT) transgene con

71 carcinogens and the protective effect of O6-methylguanine DNA methyltransferase (MGMT), heterozygous

72 Gene transfer of the AGT gene, methylguanine DNA methyltransferase (MGMT), results in o

73 ction of four different proteins, avidin, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag, an

74 plished in mammalian cells by the protein O6-methylguanine DNA methyltransferase (MGMT).

75 chors capable of covalent attachment to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusion pr

76 ease protein resulted in the retention of O6-methylguanine DNA methyltransferase activity but loss of

77 se results demonstrate that the fusion of O6-methylguanine DNA methyltransferase and apurinic endonuc

78 cted a human fusion protein consisting of O6-methylguanine DNA methyltransferase coupled with an apur

79 We observed that O (6)-methylguanine DNA methyltransferase is effective in remo

80 MGMT (O(6)-methylguanine DNA methyltransferase) and APNG (alkylpuri

81 the apurinic endonuclease portion of the O6-methylguanine DNA methyltransferase-apurinic endonucleas

82 ture-function information about the human O6-methylguanine-DNA methyltransferase (EC 2.1.1.63), as we

83 O6-methylguanine-DNA methyltransferase (MGMT [OMIM 156569])

84 l-mediated delivery of the P140K mutant O(6)-methylguanine-DNA methyltransferase (MGMT(P140K)) into h

85 O-6-methylguanine-DNA methyltransferase (MGMT) activity is d

86 Pretreatment leukemia cell O6-methylguanine-DNA methyltransferase (MGMT) activity, tum

87 liomas expressing the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) are resistant

88 a vector containing or lacking the human O6-methylguanine-DNA methyltransferase (MGMT) cDNA.

89 The repair of TMZ-induced DNA damage by O-6-methylguanine-DNA methyltransferase (MGMT) confers one m

90 The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) confers resis

91 evel expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) correlates wi

92 he p16(INK4a) tumor suppressor gene and O(6)-methylguanine-DNA methyltransferase (MGMT) DNA repair ge

93 Patients with unmethylated O(6)-methylguanine-DNA methyltransferase (MGMT) fare worse, p

94 O6-methylguanine-DNA methyltransferase (MGMT) functions to

95 The O6-methylguanine-DNA methyltransferase (MGMT) gene methylat

96 Expression of the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) in tumor corr

97 The DNA-repair enzyme O6-methylguanine-DNA methyltransferase (MGMT) inhibits the

98 O(6)-Methylguanine-DNA methyltransferase (MGMT) is a DNA repa

99 The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is a major de

100 O(6)-methylguanine-DNA methyltransferase (MGMT) is an enzyme

101 The DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT) is commonly o

102 umors (NETs) when the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) is inactivate

103 The O-6-methylguanine-DNA methyltransferase (MGMT) is responsibl

104 mechanism whereby the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is silenced i

105 O(6)-methylguanine-DNA methyltransferase (MGMT) methylation s

106 rt survival times, even in patients with O-6-Methylguanine-DNA Methyltransferase (MGMT) methylation.

107 evated expression of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) or a defect i

108 onged survival, but only in patients with O6-methylguanine-DNA methyltransferase (MGMT) promoter meth

109 Tumor tissue was assayed to determine O(6)-methylguanine-DNA methyltransferase (MGMT) promoter meth

110 methylation data from a CpG island in the O6-methylguanine-DNA methyltransferase (MGMT) promoter.

111 ion in the disposition of the inactivated O6-methylguanine-DNA methyltransferase (MGMT) protein in hu

112 he role of the promoter methylation of O (6)-methylguanine-DNA methyltransferase (MGMT) remains contr

113 The DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) removes mutag

114 O(6)-methylguanine-DNA methyltransferase (MGMT) repairs the m

115 O6-methylguanine-DNA methyltransferase (MGMT) reverses alky

116 O(6)-Methylguanine-DNA methyltransferase (MGMT) status, as pr

117 suppressed methylation at the promoter of O6-methylguanine-DNA methyltransferase (MGMT) to enhance MG

118 e methylation status of the promoter of O(6)-methylguanine-DNA methyltransferase (MGMT) was assessed.

119 O(6)-Methylguanine-DNA methyltransferase (MGMT)(1), a ubiquit

120 O6-Methylguanine-DNA methyltransferase (MGMT), a constituti

121 We have previously shown that O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair

122 he context of the targeted knockdown of O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair

123 stabilized methyltransferases, chiefly O(6)-methylguanine-DNA methyltransferase (MGMT), a key enzyme

124 O6-methylguanine-DNA methyltransferase (MGMT), a ubiquitous

125 O6-Methylguanine-DNA methyltransferase (MGMT), a ubiquitous

126 ncreased levels of the DNA repair protein O6 methylguanine-DNA methyltransferase (MGMT), also referre

127 O6-Methylguanine-DNA methyltransferase (MGMT), an enzyme th

128 errant promoter methylation of the p16, O(6)-methylguanine-DNA methyltransferase (MGMT), death-associ

129 This lesion is repaired by O6-methylguanine-DNA methyltransferase (MGMT), the expressi

130 sion of the DNA damage reversal protein O(6)-methylguanine-DNA methyltransferase (MGMT), which protec

131 atives is countered by the repair protein O6-methylguanine-DNA methyltransferase (MGMT), which remove

132 required for the cytotoxic response of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficient mam

133 ts with microsatellite-stable (MSS) and O(6)-methylguanine-DNA methyltransferase (MGMT)-silenced meta

134 MeG, a DNA lesion repaired by the protein O6-methylguanine-DNA methyltransferase (MGMT).

135 reversal mechanism by a protein termed O(6)-methylguanine-DNA methyltransferase (MGMT).

136 he normal cell by the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT).

137 mechanisms may be the high expression of O6-methylguanine-DNA methyltransferase (MGMT).

138 n receptor (ER), E-cadherin (ECAD) and O (6)-methylguanine-DNA methyltransferase (MGMT)] examined.

139 the P140K mutant of the DNA repair enzyme O6-methylguanine-DNA methyltransferase (MGMT*).

140 be attributed to the down-regulation of O(6)-methylguanine-DNA methyltransferase activity.

141 (methylated in tumor 1), MINT2, MINT31, O(6)-methylguanine-DNA methyltransferase gene, and hMLH1 mism

142 hat for three genes (P16, MLH1, and the O(6)-methylguanine-DNA methyltransferase gene, MGMT), histone

143 een limited to the methylation status of O-6-methylguanine-DNA methyltransferase in patients with gli

144 epatocyte growth factor or unmethylated O(6)-methylguanine-DNA methyltransferase may benefit from Ona

145 f GBM, including age, performance status, O6-methylguanine-DNA methyltransferase methylation, and ext

146 of MET ligand hepatocyte growth factor, O(6)-methylguanine-DNA methyltransferase promoter methylation

147 ate analysis, the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylation

148 ioblastoma that harbors a nonmethylated O(6)-methylguanine-DNA methyltransferase promotor, standard t

149 tumors, which do not express measurable O(6)-methylguanine-DNA methyltransferase protein, is probably

150 prognostic significance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and TTP

151 identified in GBMs, except for loss of O(6-)methylguanine-DNA methyltransferase via promoter methyla

152 he percentage of patients methylated at O(6)-methylguanine-DNA methyltransferase was lower than on th

153 onal 39 kDa Escherichia coli Ada protein (O6-methylguanine-DNA methyltransferase) (EC 2.1.1.63), prod

154 , c-Jun, Rb2/p130, JAK1, p67phox, Grb2, O(6)-methylguanine-DNA methyltransferase, and Ercc-1.

155 in molecules involved in DNA repair (eg, O6-methylguanine-DNA methyltransferase, DNA topoisomerase I

156 A repair enzymes, DNA polymerase beta and O6-methylguanine-DNA methyltransferase, have been shown to

157 s coli, APC; mut-L homolog 1, MLH1; and O(6)-methylguanine-DNA methyltransferase, MGMT) by liquid chr

158 nomic stability of DDR mechanisms, including methylguanine-DNA methyltransferase-mediated repair, DNA

159 g for age, tumor size, resection extent, O-6-methylguanine-DNA methyltransferase-methylation, and iso

160 Patients with newly diagnosed O(6)-methylguanine-DNA methyltransferase-unmethylated gliobla

161 ylase, Nth protein (endonuclease III) and O6-methylguanine-DNA methyltransferase.

162 methylated bases from DNA, and suicidal O(6)-methylguanine-DNA methyltransferases to transfer alkyl g

163 DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltransferase (E.C. 2.1.1.63, MGMT

164 or gene p16 (CDKN2A), the DNA repair gene O6-methylguanine-DNA-methyltransferase (MGMT) and the putat

165 116 and HCT15 cells that highly express O(6)-methylguanine-DNA-methyltransferase (MGMT) displayed a t

166 These include the importance of O6-methylguanine-DNA-methyltransferase (MGMT) in glioblasto

167 f metalloproteinase 3 (TIMP-3), p16INK4a, O6-methylguanine-DNA-methyltransferase (MGMT), death-associ

168 O6-methylguanine-DNA-methyltransferase (MGMT), which repair

169 latter fused to the DNA repair protein O(6)-methylguanine-DNA-methyltransferase (MGMT).

170 d cells in vivo, selection based on P140K O6-methylguanine-DNA-methyltransferase (MGMT[P140K]) gene t

171 radiotherapy alone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promoter

172 prolonged OS (P = 0.005) independent of O(6)-methylguanine-DNA-methyltransferase promoter methylation

173 (P < .001) and OS (P = .048), especially in methylguanine-DNA-methyltransferase unmethylated tumors

174 -specific PCR and included: p16 (CDKN2A), O6-methylguanine-DNA-methyltransferase, glutathione S-trans

175 S-transferase P1, and the DNA repair gene O6-methylguanine-DNA-methyltransferase.

176 ed: 27% (26/95) at p16, 33% (31 of 95) at O6-methylguanine-DNA-methyltransferase; and 18% (17 of 92)

177 c effects of the TMZ-induced DNA lesion O(6)-methylguanine due to elevated expression of the repair p

178 tected for reporter constructs carrying N(2)-methylguanine even in the NER-deficient XP-A cell line,

179 ution with damaged bases 8-oxoguanine and O6-methylguanine failed to prevent BG4 binding although aff

180 idative damage, including 3-methyladenine, 7-methylguanine, hypoxanthine (Hx), and 1,N(6)-ethenoadeni

181 tein does not transfer methyl groups from O6-methylguanine in [3H]-methylated DNA but reversibly inhi

182 ylating agent MNNG to create a level of O(6)-methylguanine in cellular DNA equal to that found in nor

183 Temozolomide (TMZ) produces O(6)-methylguanine in DNA, which in turn mispairs with thymin

184 TMZ produces O6-methylguanine in DNA, which mispairs with thymine during

185 tions arise as a result of formation of O(6)-methylguanine in DNA.

186 he alkyltransferase activity in repairing O6-methylguanine in methylated DNA.

187 r of MGMT protein and increased repair of O6-methylguanine in nitrosomethylurea-treated human bronchi

188 e DNA at several locations, among which O(6)-methylguanine is believed to be the most toxic.

189 Surprisingly, 7-methylguanine is removed equally efficiently in AAG:(+/+

190 O6-Methylguanine is removed from DNA via the transfer of th

191 posite this lesion, and it bypasses the O(6)-methylguanine lesion by inserting a C or a T.

192 ing the first direct visualization of the N7-methylguanine lesion nucleobase in DNA.

193 In contrast, O(6)-methylguanine lesion used as a control does not induce s

194 he main TMZ-induced toxic DNA adduct, the O6-Methylguanine lesion.

195 li and purified to homogeneity repaired O(6)-methylguanine lesions in DNA via alkyl transfer action d

196 tributor to the endogenous formation of O(6)-methylguanine lesions in E. coli.

197 Interestingly, O(6)-methylguanine lesions when paired with either a C or T w

198 ance of 3-methyladenine, and in some cases 3-methylguanine, lesions in cellular toxicity, and the dom

199 r of the cytotoxic and mutagenic lesion O(6)-methylguanine (m(6)G) in DNA.

200 nd replication of a DNA lesion, such as O(6)-methylguanine (m(6)G), can, in principle, be influenced

201 thylthymine (m(4)T) relative to that of O(6)-methylguanine (m(6)G).

202 the well-known epsilonA and Hx substrates, 1-methylguanine (m1G) was also excised efficiently by AAG.

203 Replication in vivo across unrepaired O6-methylguanine (m6dG) lesions by mammalian DNA polymerase

204 A synthesis in vitro across site-specific O6-methylguanine (m6dG) residues by DNA polymerase beta (po

205 O(6)-Methylguanine (m6G) and abasic site TLS was examined in

206 O(6)-Methylguanine (m6G) is formed by the action of alkylatin

207 e 7,8-dihydro-8-oxoguanine (8-oxoG) and O(6)-methylguanine (m6G) lesions.

208 orm specific and stable complexes with an O6-methylguanine (m6G)-containing oligonucleotide substrate

209 We have studied the processing of O(6)-methylguanine (m6G)-containing oligonucleotides and N-me

210 ytotoxic lesions N(3)-methyladenine and N(7)-methylguanine, may contribute to TMZ resistance.

211 by Sn1 methylators has been attributed to O6-methylguanine (MeG), we have constructed nicked circular

212 he course of removing a methyl group from O6-methylguanine (meG)-DNA or O4-methylthymine (meT)-DNA.

213 ge via the formation of base-labile residues methylguanine, methoxyguanine, and 8-oxo-G.

214 ioma tumors lack the DNA repair protein O(6)-methylguanine methyl transferase (MGMT).

215 iotherapy (RT) is the overexpression of O(6)-methylguanine-methyl-transferase (MGMT) enzyme.

216 s are TMZ resistant due to overexpression of methylguanine methyltransferase (MGMT(hi)).

217 oints were overall survival, RR, safety, and methylguanine methyltransferase (MGMT) by immunohistoche

218 ine DNA alkyltransferase (AGT) from the O(6)-methylguanine methyltransferase (MGMT) cDNA, which confe

219 used an oncoretroviral vector to transfer a methylguanine methyltransferase (MGMT) drug-resistance g

220 The methylation status of the O(6)-methylguanine methyltransferase (MGMT) gene promoter has

221 We hypothesized that expression of methylguanine methyltransferase (MGMT) in the tumor woul

222 retinoic acid receptor beta (RARbeta), O(6)-methylguanine methyltransferase (MGMT), and human mutL h

223 control of erythroid regulatory elements and methylguanine methyltransferase (MGMT), driven by a cons

224 lly relevant genes, Schlafen 11 (SLFN11) and methylguanine methyltransferase (MGMT), served as indica

225 the P140K mutant of the drug resistance gene methylguanine methyltransferase (MGMT), which encodes a

226 s (FV) vector expressing the P140K mutant of methylguanine methyltransferase (MGMTP140K) for in vivo

227 In vivo selection with mutant methylguanine methyltransferase (MGMTP140K) has been pro

228 ediated by a mutant of the DNA-repair enzyme methylguanine methyltransferase could circumvent this li

229 Human TK6 cells, which are methylguanine methyltransferase deficient (MGMT(-)), wer

230 e-DNA alkyltransferase (AGT), encoded by the methylguanine methyltransferase gene [MGMT], removes the

231 Mutant forms of the DNA repair-enzyme methylguanine methyltransferase in particular have allow

232 Overexpression of methylguanine methyltransferase P140K (MGMTP140K) has be

233 chromosome 19, or 1p19q codeletion; and (c) methylguanine methyltransferase promoter methylation.

234 cell transplantation, and thus we evaluated methylguanine methyltransferase-mediated chemoprotection

235 s end joining, homologous recombination, and methylguanine methyltransferase.

236 oficient tumor cells that lack expression of methylguanine methyltransferase.

237 l gammaretrovirus vector backbone expressing methylguanine methyltransferase.

238 drive the dynamics of the DNA repair enzyme, methylguanine-methyltransferase (MGMT), that repairs tem

239 The MutSDelta800 protein binds to O6-methylguanine mismatches but not to intrastrand platinat

240 O6-methylguanine mispairs with thymine during replication,

241 cating that the mutations are formed on O(6)-methylguanine modifications.

242 he structures of the interaction between O 6-methylguanine ( O 6mG) and cytosine and thymine during r

243 y, DNA adducts of biological relevance, O(6)-methylguanine (O(6)-MeG) and O(6)-carboxymethylguanine (

244 O(6)-Methylguanine (O(6)-MeG) is a highly mutagenic DNA adduc

245 O(6)-Methylguanine (O(6)-meG) is a major mutagenic, carcinoge

246 O(6)-methylguanine (O(6)-MeG) is a miscoding DNA lesion arisi

247 nce of the signaling pathway induced by O(6)-methylguanine (O(6)-MeG) lesions is poorly understood.

248 er methylation, the MGMT enzyme removes O(6)-methylguanine (O(6)-meG) lesions.

249 des containing the known MGMT substrate O(6)-methylguanine (O(6)-MeG) or O(6)-CMG effectively inactiv

250 DNA polymerase Dpo4-catalyzed bypass of O(6)-methylguanine (O(6)-MeG) proceeds largely in an accurate

251 MAMAc), and 7-methylguanine (7-MeG) and O(6)-methylguanine (O(6)-MeG) were measured in the DNAs of va

252 rimer/templates containing guanine (G), O(6)-methylguanine (O(6)-MeG), or O(6)-benzylguanine (O(6)-Bz

253 er/template DNA containing guanine (G), O(6)-methylguanine (O(6)-MeG), or O(6)-benzylguanine (O(6)-Bz

254 O(6)-Methylguanine (O(6)-meG), which is produced in DNA follo

255 While O(6)-methylguanine (O(6)-MeG)-DNA methyltransferase (MGMT) pr

256 ed formation of the promutagenic adduct O(6)-methylguanine (O(6)-meGua) by 73 and 80%, respectively,

257 O(6)-methylguanine (O(6)-methylG) is highly mutagenic and is

258 ylating agents, which produce cytotoxic O(6)-methylguanine (O(6)-mG) DNA lesions.

259 Previous studies indicated that O(6)-methylguanine (O(6)-mG) persistence is critical for lung

260 cluding methylating agents that produce O(6)-methylguanine (O(6)MeG) adducts.

261 as triggered by the specific DNA lesion O(6)-methylguanine (O(6)MeG) and characterized by arrest of c

262 oxic, and we recently demonstrated that O(6)-methylguanine (O(6)MeG) and O(6)-chloroethylguanine (O(6

263 O(6)-methylguanine (O(6)meG) and related modifications of gua

264 Alkylation-induced O(6)-methylguanine (O(6)MeG) DNA lesions can be mutagenic or

265 to a single type of DNA lesion, namely O(6)-methylguanine (O(6)MeG).

266 O(6)-methylguanine (O(6)mG) is a potent mutagenic and procarc

267 Hence, an O:(6)-methylguanine (O:(6)meG) lesion would be inaccessible to

268 MNU produces carcinogenic O6-methylguanine (O6-meG) adducts, resulting in thymic lymp

269 ormation of human fibroblasts and whether O6-methylguanine (O6-MeG) is involved, two populations of i

270 We examined the effect of a single O6-methylguanine (O6-MeG) template residue on catalysis by

271 Uracil, O6-methylguanine (O6-meG), and 8-oxoguanine (8-oxoG) were p

272 repair of the chemosensitive DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltr

273 the O6 position of guanine in DNA to form O6-methylguanine (O6-meG).

274 resence of MeC inhibited the formation of N7-methylguanine, O6-methylguanine, and O6-pyridyloxobutylg

275 lowly, T opposite the carcinogenic lesion O6-methylguanine (O6MeG) approximately 30-fold more frequen

276 nd a monoclonal antibody which recognizes O6-methylguanine (O6MeGua).

277 , that repairs temozolomide (TMZ)-induced O6-methylguanine (O6mG) adducts.

278 protein makes critical interactions with O6-methylguanine (O6mG) at the N1- and O6-positions.

279 with the 3-position of the mutagenic base O6-methylguanine (O6mG).

280 ine and 1,N6-ethenoadenine, as well as at O6-methylguanine (O6mG).

281 nce context-dependent rate differences for 7-methylguanine of up to 185-fold from position to positio

282 basicity (GB)) of adenine, guanine, and O(6)-methylguanine (OMG) have been examined using both theore

283 We also examined O(6)-methylguanine (OMG), a highly mutagenic damaged base tha

284 The effects of substitution of O6-methylguanine on the structure and stability of a human

285 ed DNA containing the endogenous lesion O(6)-methylguanine or cigarette-smoke-derived O(6)-4-(3-pyrid

286 2) IN, the replacement of the guanine with 6-methylguanine or hypoxanthine not only reduced 3'-proces

287 , and no detectable activity in repairing N1-methylguanine or N3-methylthymine.

288 The N7-methylguanine portion of the mRNA cap structure interact

289 PvuII is inhibited by O6-methylguanine, positioned within the restriction site.

290 adenine, 7-methylguanine, 3-methyladenine, 3-methylguanine, purine, 6-chloropurine, xanthine) that ha

291 AGT repairs O6-methylguanine; PvuII cleaves at its restriction site, yi

292 Rates of 7-methylguanine repair showed a 30-fold dependence on nucl

293 We quantified the number of O6-methylguanine residues in methylated DNA by HPLC-MS/MS a

294 ltransferase compete for the MNNG-induced O6-methylguanine residues, and MMR-induced cytotoxicity is

295 These results suggest that O(6)-methylguanine uniquely activates the molecular switch fu

296 ates of deamination of 9-methyladenine and 9-methylguanine were found to be similar to each other (t1

297 Higher relative concentrations of 7-methylguanine were observed in urine specimens from Thai

298 of the NOC-specific DNA adduct O(6)-carboxy-methylguanine when pork underwent a more intense heating

299 er oligodeoxyribonucleotides containing O(6)-methylguanine, where a minimum of four nucleotides 3' to

300 lkylated bases such as 3-methyladenine and 7-methylguanine whereas methyl-formamidopyrimidine was exc