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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 g-Cpr-null mice correlated with reduced lung O6-methylguanine adduct levels, without decreases in NNK
7 lting in a fully functional protein for both O6-methylguanine and apurinic/apyrimidinic (AP) site rep
8 hesis across SOS-independent lesions such as O6-methylguanine and DNA uracil is around 90%, very clos
9 oplatinum(II), as well as base pairs between O6-methylguanine and thymine or cytosine, or between O4-
10 ecognize certain forms of DNA damage such as O6-methylguanine and UV photoproducts, and, therefore, m
11 inhibited the formation of N7-methylguanine, O6-methylguanine, and O6-pyridyloxobutylguanine at a nei
12 (c) bind to oligodeoxynucleotides containing O6-methylguanine; and (d) react with the low molecular w
14 th LMO1 and MGMT, and thereby able to repair O6-methylguanine DNA adducts induced by MNU, would be pr
15 omain family protein 1A (RASSF1A) (57%), and O6-methylguanine DNA methylatransferase (MGMT) (34%), an
18 etinoic acid receptor-beta2 (RAR-beta2), and O6-methylguanine DNA methyltransferase (MGMT) genes were
20 of the gene encoding the DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) might be r
21 ow cells express extremely low levels of the O6-methylguanine DNA methyltransferase (MGMT) protein th
25 tal carcinogens and the protective effect of O6-methylguanine DNA methyltransferase (MGMT), heterozyg
26 etection of four different proteins, avidin, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag,
28 uclease protein resulted in the retention of O6-methylguanine DNA methyltransferase activity but loss
29 These results demonstrate that the fusion of O6-methylguanine DNA methyltransferase and apurinic endo
30 tructed a human fusion protein consisting of O6-methylguanine DNA methyltransferase coupled with an a
31 of the apurinic endonuclease portion of the O6-methylguanine DNA methyltransferase-apurinic endonucl
32 t increased levels of the DNA repair protein O6 methylguanine-DNA methyltransferase (MGMT), also refe
33 ructure-function information about the human O6-methylguanine-DNA methyltransferase (EC 2.1.1.63), as
37 h-level expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) correlates
42 The mechanism whereby the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is silence
43 ed methylation data from a CpG island in the O6-methylguanine-DNA methyltransferase (MGMT) promoter.
44 nation in the disposition of the inactivated O6-methylguanine-DNA methyltransferase (MGMT) protein in
51 rivatives is countered by the repair protein O6-methylguanine-DNA methyltransferase (MGMT), which rem
55 ariate analysis, the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylat
56 wed prognostic significance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and
57 ctional 39 kDa Escherichia coli Ada protein (O6-methylguanine-DNA methyltransferase) (EC 2.1.1.63), p
58 ges in molecules involved in DNA repair (eg, O6-methylguanine-DNA methyltransferase, DNA topoisomeras
59 DNA repair enzymes, DNA polymerase beta and O6-methylguanine-DNA methyltransferase, have been shown
61 ve DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltransferase (E.C. 2.1.1.63, M
62 essor gene p16 (CDKN2A), the DNA repair gene O6-methylguanine-DNA-methyltransferase (MGMT) and the pu
64 r of metalloproteinase 3 (TIMP-3), p16INK4a, O6-methylguanine-DNA-methyltransferase (MGMT), death-ass
66 uced cells in vivo, selection based on P140K O6-methylguanine-DNA-methyltransferase (MGMT[P140K]) gen
67 or radiotherapy alone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promo
68 ion-specific PCR and included: p16 (CDKN2A), O6-methylguanine-DNA-methyltransferase, glutathione S-tr
70 udied: 27% (26/95) at p16, 33% (31 of 95) at O6-methylguanine-DNA-methyltransferase; and 18% (17 of 9
71 protein does not transfer methyl groups from O6-methylguanine in [3H]-methylated DNA but reversibly i
74 over of MGMT protein and increased repair of O6-methylguanine in nitrosomethylurea-treated human bron
77 DNA synthesis in vitro across site-specific O6-methylguanine (m6dG) residues by DNA polymerase beta
78 o form specific and stable complexes with an O6-methylguanine (m6G)-containing oligonucleotide substr
79 ng by Sn1 methylators has been attributed to O6-methylguanine (MeG), we have constructed nicked circu
80 n the course of removing a methyl group from O6-methylguanine (meG)-DNA or O4-methylthymine (meT)-DNA
84 nsformation of human fibroblasts and whether O6-methylguanine (O6-MeG) is involved, two populations o
87 the repair of the chemosensitive DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methy
89 t slowly, T opposite the carcinogenic lesion O6-methylguanine (O6MeG) approximately 30-fold more freq
91 Ada protein makes critical interactions with O6-methylguanine (O6mG) at the N1- and O6-positions.
98 thyltransferase compete for the MNNG-induced O6-methylguanine residues, and MMR-induced cytotoxicity
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