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1 key role in the interaction with the flipped O6-methylguanine.
2 e containing O6-benzylguanine and the other, O6-methylguanine.
3 le-stranded oligodeoxynucleotides containing O6-methylguanine.
4 most cytotoxic of lesions generated by TMZ, O(6)-methylguanine.
5 dem mass spectrometry analysis of unrepaired O(6)-methylguanine.
6 influenced by sequence context than that of O(6)-methylguanine.
7 , we examine the functions of this enzyme on O(6)-methylguanine (6mG) adducts in the four-stranded st
8 alkyltransferase (AGT) show that it forms an O(6)-methylguanine (6mG)-specific complex on duplex DNA
9 nucleotides containing a single well defined O(6)-methylguanine adduct were used to examine the exten
10 g-Cpr-null mice correlated with reduced lung O6-methylguanine adduct levels, without decreases in NNK
17 sensitized cells to the cytotoxic DNA lesion O(6)-methylguanine and caused a synthetic lethal interac
18 -1-(3-pyridyl)-1-butanone-induced short-term O(6)-methylguanine and long-term adenoma formation in th
19 o-N-nitrosoguanidine (MNNG), which generates O(6)-methylguanine and O(4)-methylthymine recognized by
20 lting in a fully functional protein for both O6-methylguanine and apurinic/apyrimidinic (AP) site rep
21 hesis across SOS-independent lesions such as O6-methylguanine and DNA uracil is around 90%, very clos
22 oplatinum(II), as well as base pairs between O6-methylguanine and thymine or cytosine, or between O4-
23 ecognize certain forms of DNA damage such as O6-methylguanine and UV photoproducts, and, therefore, m
24 ting a C residue opposite an abasic site, an O(6)-methylguanine, and an 8-oxoguanine lesion, respecti
25 inhibited the formation of N7-methylguanine, O6-methylguanine, and O6-pyridyloxobutylguanine at a nei
26 (c) bind to oligodeoxynucleotides containing O6-methylguanine; and (d) react with the low molecular w
29 the protein is capable of tightly binding to O(6)-methylguanine-containing DNA and disrupting its rep
30 work showed that, in addition to changes in O(6)-methylguanine DNA methyltransferase (MGMT) activity
31 itative measurement of alkylation repair via O(6)-methylguanine DNA methyltransferase (MGMT) and base
33 en used in this study to specifically target O(6)-methylguanine DNA methyltransferase (MGMT) to the m
34 id anchors capable of covalent attachment to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusi
36 th LMO1 and MGMT, and thereby able to repair O6-methylguanine DNA adducts induced by MNU, would be pr
37 omain family protein 1A (RASSF1A) (57%), and O6-methylguanine DNA methylatransferase (MGMT) (34%), an
40 etinoic acid receptor-beta2 (RAR-beta2), and O6-methylguanine DNA methyltransferase (MGMT) genes were
42 of the gene encoding the DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) might be r
43 ow cells express extremely low levels of the O6-methylguanine DNA methyltransferase (MGMT) protein th
47 tal carcinogens and the protective effect of O6-methylguanine DNA methyltransferase (MGMT), heterozyg
48 etection of four different proteins, avidin, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag,
50 uclease protein resulted in the retention of O6-methylguanine DNA methyltransferase activity but loss
51 These results demonstrate that the fusion of O6-methylguanine DNA methyltransferase and apurinic endo
52 tructed a human fusion protein consisting of O6-methylguanine DNA methyltransferase coupled with an a
53 of the apurinic endonuclease portion of the O6-methylguanine DNA methyltransferase-apurinic endonucl
54 oviral-mediated delivery of the P140K mutant O(6)-methylguanine-DNA methyltransferase (MGMT(P140K)) i
55 er, gliomas expressing the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) are resi
56 of the p16(INK4a) tumor suppressor gene and O(6)-methylguanine-DNA methyltransferase (MGMT) DNA repa
61 ine tumors (NETs) when the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) is inact
63 to elevated expression of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) or a def
67 The methylation status of the promoter of O(6)-methylguanine-DNA methyltransferase (MGMT) was asse
70 in the context of the targeted knockdown of O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA r
71 d and stabilized methyltransferases, chiefly O(6)-methylguanine-DNA methyltransferase (MGMT), a key e
72 or aberrant promoter methylation of the p16, O(6)-methylguanine-DNA methyltransferase (MGMT), death-a
73 n version of the DNA damage reversal protein O(6)-methylguanine-DNA methyltransferase (MGMT), which p
74 also required for the cytotoxic response of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficien
75 atients with microsatellite-stable (MSS) and O(6)-methylguanine-DNA methyltransferase (MGMT)-silenced
79 INT1 (methylated in tumor 1), MINT2, MINT31, O(6)-methylguanine-DNA methyltransferase gene, and hMLH1
80 ion that for three genes (P16, MLH1, and the O(6)-methylguanine-DNA methyltransferase gene, MGMT), hi
81 of hepatocyte growth factor or unmethylated O(6)-methylguanine-DNA methyltransferase may benefit fro
82 vels of MET ligand hepatocyte growth factor, O(6)-methylguanine-DNA methyltransferase promoter methyl
83 ed glioblastoma that harbors a nonmethylated O(6)-methylguanine-DNA methyltransferase promotor, stand
84 D-54 tumors, which do not express measurable O(6)-methylguanine-DNA methyltransferase protein, is pro
86 ELF3, c-Jun, Rb2/p130, JAK1, p67phox, Grb2, O(6)-methylguanine-DNA methyltransferase, and Ercc-1.
87 yposis coli, APC; mut-L homolog 1, MLH1; and O(6)-methylguanine-DNA methyltransferase, MGMT) by liqui
89 some methylated bases from DNA, and suicidal O(6)-methylguanine-DNA methyltransferases to transfer al
90 HCT116 and HCT15 cells that highly express O(6)-methylguanine-DNA-methyltransferase (MGMT) displaye
91 ward tumors that lack the DNA repair protein O(6)-methylguanine-DNA-methyltransferase (MGMT), which r
93 TV a prolonged OS (P = 0.005) independent of O(6)-methylguanine-DNA-methyltransferase promoter methyl
94 been identified in GBMs, except for loss of O(6-)methylguanine-DNA methyltransferase via promoter me
95 t increased levels of the DNA repair protein O6 methylguanine-DNA methyltransferase (MGMT), also refe
96 ructure-function information about the human O6-methylguanine-DNA methyltransferase (EC 2.1.1.63), as
101 h-level expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) correlates
107 The mechanism whereby the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is silence
108 rolonged survival, but only in patients with O6-methylguanine-DNA methyltransferase (MGMT) promoter m
109 ed methylation data from a CpG island in the O6-methylguanine-DNA methyltransferase (MGMT) promoter.
110 nation in the disposition of the inactivated O6-methylguanine-DNA methyltransferase (MGMT) protein in
113 ut suppressed methylation at the promoter of O6-methylguanine-DNA methyltransferase (MGMT) to enhance
119 rivatives is countered by the repair protein O6-methylguanine-DNA methyltransferase (MGMT), which rem
123 s of GBM, including age, performance status, O6-methylguanine-DNA methyltransferase methylation, and
124 ariate analysis, the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylat
125 wed prognostic significance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and
126 ctional 39 kDa Escherichia coli Ada protein (O6-methylguanine-DNA methyltransferase) (EC 2.1.1.63), p
127 ges in molecules involved in DNA repair (eg, O6-methylguanine-DNA methyltransferase, DNA topoisomeras
128 DNA repair enzymes, DNA polymerase beta and O6-methylguanine-DNA methyltransferase, have been shown
130 ve DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltransferase (E.C. 2.1.1.63, M
131 essor gene p16 (CDKN2A), the DNA repair gene O6-methylguanine-DNA-methyltransferase (MGMT) and the pu
133 r of metalloproteinase 3 (TIMP-3), p16INK4a, O6-methylguanine-DNA-methyltransferase (MGMT), death-ass
135 uced cells in vivo, selection based on P140K O6-methylguanine-DNA-methyltransferase (MGMT[P140K]) gen
136 or radiotherapy alone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promo
137 ion-specific PCR and included: p16 (CDKN2A), O6-methylguanine-DNA-methyltransferase, glutathione S-tr
139 udied: 27% (26/95) at p16, 33% (31 of 95) at O6-methylguanine-DNA-methyltransferase; and 18% (17 of 9
140 otoxic effects of the TMZ-induced DNA lesion O(6)-methylguanine due to elevated expression of the rep
141 titution with damaged bases 8-oxoguanine and O6-methylguanine failed to prevent BG4 binding although
142 methylating agent MNNG to create a level of O(6)-methylguanine in cellular DNA equal to that found i
145 protein does not transfer methyl groups from O6-methylguanine in [3H]-methylated DNA but reversibly i
148 over of MGMT protein and increased repair of O6-methylguanine in nitrosomethylurea-treated human bron
149 kylate DNA at several locations, among which O(6)-methylguanine is believed to be the most toxic.
154 ia coli and purified to homogeneity repaired O(6)-methylguanine lesions in DNA via alkyl transfer act
158 ir, and replication of a DNA lesion, such as O(6)-methylguanine (m(6)G), can, in principle, be influe
161 DNA synthesis in vitro across site-specific O6-methylguanine (m6dG) residues by DNA polymerase beta
166 o form specific and stable complexes with an O6-methylguanine (m6G)-containing oligonucleotide substr
167 ng by Sn1 methylators has been attributed to O6-methylguanine (MeG), we have constructed nicked circu
168 n the course of removing a methyl group from O6-methylguanine (meG)-DNA or O4-methylthymine (meT)-DNA
170 d radiotherapy (RT) is the overexpression of O(6)-methylguanine-methyl-transferase (MGMT) enzyme.
171 lguanine DNA alkyltransferase (AGT) from the O(6)-methylguanine methyltransferase (MGMT) cDNA, which
173 K4a), retinoic acid receptor beta (RARbeta), O(6)-methylguanine methyltransferase (MGMT), and human m
177 study, DNA adducts of biological relevance, O(6)-methylguanine (O(6)-MeG) and O(6)-carboxymethylguan
181 ificance of the signaling pathway induced by O(6)-methylguanine (O(6)-MeG) lesions is poorly understo
183 leotides containing the known MGMT substrate O(6)-methylguanine (O(6)-MeG) or O(6)-CMG effectively in
184 icus DNA polymerase Dpo4-catalyzed bypass of O(6)-methylguanine (O(6)-MeG) proceeds largely in an acc
185 ate (MAMAc), and 7-methylguanine (7-MeG) and O(6)-methylguanine (O(6)-MeG) were measured in the DNAs
186 of primer/templates containing guanine (G), O(6)-methylguanine (O(6)-MeG), or O(6)-benzylguanine (O(
187 primer/template DNA containing guanine (G), O(6)-methylguanine (O(6)-MeG), or O(6)-benzylguanine (O(
190 hibited formation of the promutagenic adduct O(6)-methylguanine (O(6)-meGua) by 73 and 80%, respectiv
195 nce was triggered by the specific DNA lesion O(6)-methylguanine (O(6)MeG) and characterized by arrest
196 cytotoxic, and we recently demonstrated that O(6)-methylguanine (O(6)MeG) and O(6)-chloroethylguanine
202 nsformation of human fibroblasts and whether O6-methylguanine (O6-MeG) is involved, two populations o
205 the repair of the chemosensitive DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methy
207 t slowly, T opposite the carcinogenic lesion O6-methylguanine (O6MeG) approximately 30-fold more freq
210 Ada protein makes critical interactions with O6-methylguanine (O6mG) at the N1- and O6-positions.
213 hase basicity (GB)) of adenine, guanine, and O(6)-methylguanine (OMG) have been examined using both t
216 damaged DNA containing the endogenous lesion O(6)-methylguanine or cigarette-smoke-derived O(6)-4-(3-
220 thyltransferase compete for the MNNG-induced O6-methylguanine residues, and MMR-induced cytotoxicity
222 16-mer oligodeoxyribonucleotides containing O(6)-methylguanine, where a minimum of four nucleotides