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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 cytotoxic of lesions generated by TMZ, O(6)-methylguanine.
11 ass spectrometry analysis of unrepaired O(6)-methylguanine.
12 f AlkA purine substrates (7-methyladenine, 7-methylguanine, 3-methyladenine, 3-methylguanine, purine,
13 examine the functions of this enzyme on O(6)-methylguanine (6mG) adducts in the four-stranded structu
14 transferase (AGT) show that it forms an O(6)-methylguanine (6mG)-specific complex on duplex DNA that
15 or methylazoxymethyl acetate (MAMAc), and 7-methylguanine (7-MeG) and O(6)-methylguanine (O(6)-MeG)
16 mals to release 3-methyladenine (3-meA) or 7-methylguanine (7-meG) from 3H-methylated calf thymus DNA
18 nd purine, whereas YjcD and YgfQ recognize 1-methylguanine, 8-azaguanine, 6-thioguanine, and 6-mercap
19 t, the pH-rate profile for the reaction of 7-methylguanine, a positively charged substrate, shows onl
20 pr-null mice correlated with reduced lung O6-methylguanine adduct levels, without decreases in NNK bi
21 otides containing a single well defined O(6)-methylguanine adduct were used to examine the extent of
22 This work shows a mechanism whereby O(6)-methylguanine adducts formed by temozolomide lead to inh
23 The ability of temozolomide to form O(6)-methylguanine adducts is important for inhibition of NF-
24 methyl sulfate-induced 3-methyladenine and 7-methylguanine adducts were measured at nucleotide resolu
30 ng in a fully functional protein for both O6-methylguanine and apurinic/apyrimidinic (AP) site repair
31 tized cells to the cytotoxic DNA lesion O(6)-methylguanine and caused a synthetic lethal interaction
32 is across SOS-independent lesions such as O6-methylguanine and DNA uracil is around 90%, very close t
33 -pyridyl)-1-butanone-induced short-term O(6)-methylguanine and long-term adenoma formation in the lun
34 gh a majority of the TMZ-induced lesions (N7-methylguanine and N3-methyladenine) are base excision re
36 itrosoguanidine (MNNG), which generates O(6)-methylguanine and O(4)-methylthymine recognized by MMR s
37 atinum(II), as well as base pairs between O6-methylguanine and thymine or cytosine, or between O4-met
38 gnize certain forms of DNA damage such as O6-methylguanine and UV photoproducts, and, therefore, mism
39 a C residue opposite an abasic site, an O(6)-methylguanine, and an 8-oxoguanine lesion, respectively.
41 ibited the formation of N7-methylguanine, O6-methylguanine, and O6-pyridyloxobutylguanine at a neighb
42 bind to oligodeoxynucleotides containing O6-methylguanine; and (d) react with the low molecular weig
45 ro excision data indicates that removal of 7-methylguanine by the MPG protein is the rate-limiting st
47 most methylating agents (which form mainly 7-methylguanine), can specifically induce sister chromatid
48 ukaryotes is the addition of a 5'-terminal 7-methylguanine cap (m7GpppN) to nascent pre-mRNAs in the
49 rotein is capable of tightly binding to O(6)-methylguanine-containing DNA and disrupting its repair b
51 LMO1 and MGMT, and thereby able to repair O6-methylguanine DNA adducts induced by MNU, would be prote
52 in family protein 1A (RASSF1A) (57%), and O6-methylguanine DNA methylatransferase (MGMT) (34%), and d
53 showed that, in addition to changes in O(6)-methylguanine DNA methyltransferase (MGMT) activity, sma
54 ve measurement of alkylation repair via O(6)-methylguanine DNA methyltransferase (MGMT) and base exci
56 l inactivation of the non-X-linked human O-6-methylguanine DNA methyltransferase (MGMT) gene has been
58 noic acid receptor-beta2 (RAR-beta2), and O6-methylguanine DNA methyltransferase (MGMT) genes were as
60 the gene encoding the DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) might be redu
61 cells express extremely low levels of the O6-methylguanine DNA methyltransferase (MGMT) protein that
66 ed in this study to specifically target O(6)-methylguanine DNA methyltransferase (MGMT) to the mitoch
67 carcinogens and the protective effect of O6-methylguanine DNA methyltransferase (MGMT), heterozygous
69 ction of four different proteins, avidin, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag, an
71 chors capable of covalent attachment to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusion pr
72 ease protein resulted in the retention of O6-methylguanine DNA methyltransferase activity but loss of
73 se results demonstrate that the fusion of O6-methylguanine DNA methyltransferase and apurinic endonuc
74 cted a human fusion protein consisting of O6-methylguanine DNA methyltransferase coupled with an apur
76 the apurinic endonuclease portion of the O6-methylguanine DNA methyltransferase-apurinic endonucleas
77 ture-function information about the human O6-methylguanine-DNA methyltransferase (EC 2.1.1.63), as we
78 l-mediated delivery of the P140K mutant O(6)-methylguanine-DNA methyltransferase (MGMT(P140K)) into h
80 liomas expressing the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) are resistant
82 The repair of TMZ-induced DNA damage by O-6-methylguanine-DNA methyltransferase (MGMT) confers one m
84 evel expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) correlates wi
85 he p16(INK4a) tumor suppressor gene and O(6)-methylguanine-DNA methyltransferase (MGMT) DNA repair ge
88 Expression of the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) in tumor corr
93 mechanism whereby the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is silenced i
95 evated expression of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) or a defect i
96 Tumor tissue was assayed to determine O(6)-methylguanine-DNA methyltransferase (MGMT) promoter meth
97 methylation data from a CpG island in the O6-methylguanine-DNA methyltransferase (MGMT) promoter.
98 ion in the disposition of the inactivated O6-methylguanine-DNA methyltransferase (MGMT) protein in hu
99 he role of the promoter methylation of O (6)-methylguanine-DNA methyltransferase (MGMT) remains contr
102 e methylation status of the promoter of O(6)-methylguanine-DNA methyltransferase (MGMT) was assessed.
106 he context of the targeted knockdown of O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA repair
107 stabilized methyltransferases, chiefly O(6)-methylguanine-DNA methyltransferase (MGMT), a key enzyme
110 ncreased levels of the DNA repair protein O6 methylguanine-DNA methyltransferase (MGMT), also referre
112 errant promoter methylation of the p16, O(6)-methylguanine-DNA methyltransferase (MGMT), death-associ
114 sion of the DNA damage reversal protein O(6)-methylguanine-DNA methyltransferase (MGMT), which protec
115 atives is countered by the repair protein O6-methylguanine-DNA methyltransferase (MGMT), which remove
116 required for the cytotoxic response of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficient mam
121 n receptor (ER), E-cadherin (ECAD) and O (6)-methylguanine-DNA methyltransferase (MGMT)] examined.
124 (methylated in tumor 1), MINT2, MINT31, O(6)-methylguanine-DNA methyltransferase gene, and hMLH1 mism
125 hat for three genes (P16, MLH1, and the O(6)-methylguanine-DNA methyltransferase gene, MGMT), histone
126 een limited to the methylation status of O-6-methylguanine-DNA methyltransferase in patients with gli
127 epatocyte growth factor or unmethylated O(6)-methylguanine-DNA methyltransferase may benefit from Ona
128 of MET ligand hepatocyte growth factor, O(6)-methylguanine-DNA methyltransferase promoter methylation
129 ate analysis, the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylation
130 ioblastoma that harbors a nonmethylated O(6)-methylguanine-DNA methyltransferase promotor, standard t
131 tumors, which do not express measurable O(6)-methylguanine-DNA methyltransferase protein, is probably
132 prognostic significance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and TTP
133 identified in GBMs, except for loss of O(6-)methylguanine-DNA methyltransferase via promoter methyla
134 he percentage of patients methylated at O(6)-methylguanine-DNA methyltransferase was lower than on th
135 onal 39 kDa Escherichia coli Ada protein (O6-methylguanine-DNA methyltransferase) (EC 2.1.1.63), prod
137 in molecules involved in DNA repair (eg, O6-methylguanine-DNA methyltransferase, DNA topoisomerase I
138 A repair enzymes, DNA polymerase beta and O6-methylguanine-DNA methyltransferase, have been shown to
139 s coli, APC; mut-L homolog 1, MLH1; and O(6)-methylguanine-DNA methyltransferase, MGMT) by liquid chr
140 g for age, tumor size, resection extent, O-6-methylguanine-DNA methyltransferase-methylation, and iso
142 methylated bases from DNA, and suicidal O(6)-methylguanine-DNA methyltransferases to transfer alkyl g
143 DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltransferase (E.C. 2.1.1.63, MGMT
144 or gene p16 (CDKN2A), the DNA repair gene O6-methylguanine-DNA-methyltransferase (MGMT) and the putat
145 116 and HCT15 cells that highly express O(6)-methylguanine-DNA-methyltransferase (MGMT) displayed a t
147 f metalloproteinase 3 (TIMP-3), p16INK4a, O6-methylguanine-DNA-methyltransferase (MGMT), death-associ
150 d cells in vivo, selection based on P140K O6-methylguanine-DNA-methyltransferase (MGMT[P140K]) gene t
151 radiotherapy alone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promoter
152 -specific PCR and included: p16 (CDKN2A), O6-methylguanine-DNA-methyltransferase, glutathione S-trans
154 ed: 27% (26/95) at p16, 33% (31 of 95) at O6-methylguanine-DNA-methyltransferase; and 18% (17 of 92)
155 c effects of the TMZ-induced DNA lesion O(6)-methylguanine due to elevated expression of the repair p
156 idative damage, including 3-methyladenine, 7-methylguanine, hypoxanthine (Hx), and 1,N(6)-ethenoadeni
157 tein does not transfer methyl groups from O6-methylguanine in [3H]-methylated DNA but reversibly inhi
158 ylating agent MNNG to create a level of O(6)-methylguanine in cellular DNA equal to that found in nor
163 r of MGMT protein and increased repair of O6-methylguanine in nitrosomethylurea-treated human bronchi
169 li and purified to homogeneity repaired O(6)-methylguanine lesions in DNA via alkyl transfer action d
172 ance of 3-methyladenine, and in some cases 3-methylguanine, lesions in cellular toxicity, and the dom
174 nd replication of a DNA lesion, such as O(6)-methylguanine (m(6)G), can, in principle, be influenced
176 the well-known epsilonA and Hx substrates, 1-methylguanine (m1G) was also excised efficiently by AAG.
177 Replication in vivo across unrepaired O6-methylguanine (m6dG) lesions by mammalian DNA polymerase
178 A synthesis in vitro across site-specific O6-methylguanine (m6dG) residues by DNA polymerase beta (po
182 orm specific and stable complexes with an O6-methylguanine (m6G)-containing oligonucleotide substrate
185 by Sn1 methylators has been attributed to O6-methylguanine (MeG), we have constructed nicked circular
186 he course of removing a methyl group from O6-methylguanine (meG)-DNA or O4-methylthymine (meT)-DNA.
189 ine DNA alkyltransferase (AGT) from the O(6)-methylguanine methyltransferase (MGMT) cDNA, which confe
190 used an oncoretroviral vector to transfer a methylguanine methyltransferase (MGMT) drug-resistance g
192 retinoic acid receptor beta (RARbeta), O(6)-methylguanine methyltransferase (MGMT), and human mutL h
193 control of erythroid regulatory elements and methylguanine methyltransferase (MGMT), driven by a cons
194 lly relevant genes, Schlafen 11 (SLFN11) and methylguanine methyltransferase (MGMT), served as indica
195 the P140K mutant of the drug resistance gene methylguanine methyltransferase (MGMT), which encodes a
196 s (FV) vector expressing the P140K mutant of methylguanine methyltransferase (MGMTP140K) for in vivo
198 ediated by a mutant of the DNA-repair enzyme methylguanine methyltransferase could circumvent this li
200 e-DNA alkyltransferase (AGT), encoded by the methylguanine methyltransferase gene [MGMT], removes the
203 chromosome 19, or 1p19q codeletion; and (c) methylguanine methyltransferase promoter methylation.
204 cell transplantation, and thus we evaluated methylguanine methyltransferase-mediated chemoprotection
210 he structures of the interaction between O 6-methylguanine ( O 6mG) and cytosine and thymine during r
211 y, DNA adducts of biological relevance, O(6)-methylguanine (O(6)-MeG) and O(6)-carboxymethylguanine (
215 nce of the signaling pathway induced by O(6)-methylguanine (O(6)-MeG) lesions is poorly understood.
216 des containing the known MGMT substrate O(6)-methylguanine (O(6)-MeG) or O(6)-CMG effectively inactiv
217 DNA polymerase Dpo4-catalyzed bypass of O(6)-methylguanine (O(6)-MeG) proceeds largely in an accurate
218 MAMAc), and 7-methylguanine (7-MeG) and O(6)-methylguanine (O(6)-MeG) were measured in the DNAs of va
219 rimer/templates containing guanine (G), O(6)-methylguanine (O(6)-MeG), or O(6)-benzylguanine (O(6)-Bz
220 er/template DNA containing guanine (G), O(6)-methylguanine (O(6)-MeG), or O(6)-benzylguanine (O(6)-Bz
222 ed formation of the promutagenic adduct O(6)-methylguanine (O(6)-meGua) by 73 and 80%, respectively,
227 oxic, and we recently demonstrated that O(6)-methylguanine (O(6)MeG) and O(6)-chloroethylguanine (O(6
234 ormation of human fibroblasts and whether O6-methylguanine (O6-MeG) is involved, two populations of i
237 repair of the chemosensitive DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltr
239 resence of MeC inhibited the formation of N7-methylguanine, O6-methylguanine, and O6-pyridyloxobutylg
240 lowly, T opposite the carcinogenic lesion O6-methylguanine (O6MeG) approximately 30-fold more frequen
245 nce context-dependent rate differences for 7-methylguanine of up to 185-fold from position to positio
246 basicity (GB)) of adenine, guanine, and O(6)-methylguanine (OMG) have been examined using both theore
249 ed DNA containing the endogenous lesion O(6)-methylguanine or cigarette-smoke-derived O(6)-4-(3-pyrid
250 2) IN, the replacement of the guanine with 6-methylguanine or hypoxanthine not only reduced 3'-proces
254 adenine, 7-methylguanine, 3-methyladenine, 3-methylguanine, purine, 6-chloropurine, xanthine) that ha
258 ltransferase compete for the MNNG-induced O6-methylguanine residues, and MMR-induced cytotoxicity is
260 ates of deamination of 9-methyladenine and 9-methylguanine were found to be similar to each other (t1
261 of the NOC-specific DNA adduct O(6)-carboxy-methylguanine when pork underwent a more intense heating
262 er oligodeoxyribonucleotides containing O(6)-methylguanine, where a minimum of four nucleotides 3' to
263 lkylated bases such as 3-methyladenine and 7-methylguanine whereas methyl-formamidopyrimidine was exc
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