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1 cosylase, Nth protein (endonuclease III) and O6-methylguanine-DNA methyltransferase.
2 ne S-transferase P1, and the DNA repair gene O6-methylguanine-DNA-methyltransferase.
4 uclease protein resulted in the retention of O6-methylguanine DNA methyltransferase activity but loss
5 These results demonstrate that the fusion of O6-methylguanine DNA methyltransferase and apurinic endo
8 udied: 27% (26/95) at p16, 33% (31 of 95) at O6-methylguanine-DNA-methyltransferase; and 18% (17 of 9
9 of the apurinic endonuclease portion of the O6-methylguanine DNA methyltransferase-apurinic endonucl
10 tructed a human fusion protein consisting of O6-methylguanine DNA methyltransferase coupled with an a
11 ges in molecules involved in DNA repair (eg, O6-methylguanine-DNA methyltransferase, DNA topoisomeras
12 ve DNA lesion, O6-methylguanine (O6-MeG), by O6-methylguanine-DNA-methyltransferase (E.C. 2.1.1.63, M
13 ructure-function information about the human O6-methylguanine-DNA methyltransferase (EC 2.1.1.63), as
14 ctional 39 kDa Escherichia coli Ada protein (O6-methylguanine-DNA methyltransferase) (EC 2.1.1.63), p
15 INT1 (methylated in tumor 1), MINT2, MINT31, O(6)-methylguanine-DNA methyltransferase gene, and hMLH1
16 ion that for three genes (P16, MLH1, and the O(6)-methylguanine-DNA methyltransferase gene, MGMT), hi
17 or radiotherapy alone, with consideration of O6-methylguanine-DNA-methyltransferase gene (MGMT) promo
18 ion-specific PCR and included: p16 (CDKN2A), O6-methylguanine-DNA-methyltransferase, glutathione S-tr
19 DNA repair enzymes, DNA polymerase beta and O6-methylguanine-DNA methyltransferase, have been shown
20 of hepatocyte growth factor or unmethylated O(6)-methylguanine-DNA methyltransferase may benefit fro
21 s of GBM, including age, performance status, O6-methylguanine-DNA methyltransferase methylation, and
22 work showed that, in addition to changes in O(6)-methylguanine DNA methyltransferase (MGMT) activity
23 itative measurement of alkylation repair via O(6)-methylguanine DNA methyltransferase (MGMT) and base
25 en used in this study to specifically target O(6)-methylguanine DNA methyltransferase (MGMT) to the m
26 oviral-mediated delivery of the P140K mutant O(6)-methylguanine-DNA methyltransferase (MGMT(P140K)) i
27 er, gliomas expressing the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) are resi
28 of the p16(INK4a) tumor suppressor gene and O(6)-methylguanine-DNA methyltransferase (MGMT) DNA repa
33 ine tumors (NETs) when the DNA repair enzyme O(6)-methylguanine-DNA methyltransferase (MGMT) is inact
35 to elevated expression of the repair protein O(6)-methylguanine-DNA methyltransferase (MGMT) or a def
39 The methylation status of the promoter of O(6)-methylguanine-DNA methyltransferase (MGMT) was asse
41 in the context of the targeted knockdown of O(6)-methylguanine-DNA methyltransferase (MGMT), a DNA r
43 d and stabilized methyltransferases, chiefly O(6)-methylguanine-DNA methyltransferase (MGMT), a key e
44 or aberrant promoter methylation of the p16, O(6)-methylguanine-DNA methyltransferase (MGMT), death-a
45 n version of the DNA damage reversal protein O(6)-methylguanine-DNA methyltransferase (MGMT), which p
46 also required for the cytotoxic response of O(6)-methylguanine-DNA methyltransferase (MGMT)-deficien
47 atients with microsatellite-stable (MSS) and O(6)-methylguanine-DNA methyltransferase (MGMT)-silenced
50 HCT116 and HCT15 cells that highly express O(6)-methylguanine-DNA-methyltransferase (MGMT) displaye
51 ward tumors that lack the DNA repair protein O(6)-methylguanine-DNA-methyltransferase (MGMT), which r
53 t increased levels of the DNA repair protein O6 methylguanine-DNA methyltransferase (MGMT), also refe
56 etinoic acid receptor-beta2 (RAR-beta2), and O6-methylguanine DNA methyltransferase (MGMT) genes were
58 of the gene encoding the DNA repair protein O6-methylguanine DNA methyltransferase (MGMT) might be r
59 ow cells express extremely low levels of the O6-methylguanine DNA methyltransferase (MGMT) protein th
63 tal carcinogens and the protective effect of O6-methylguanine DNA methyltransferase (MGMT), heterozyg
64 etection of four different proteins, avidin, O6-methylguanine DNA methyltransferase (MGMT), SNAP-tag,
70 h-level expression of the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) correlates
76 The mechanism whereby the DNA repair protein O6-methylguanine-DNA methyltransferase (MGMT) is silence
77 rolonged survival, but only in patients with O6-methylguanine-DNA methyltransferase (MGMT) promoter m
78 ed methylation data from a CpG island in the O6-methylguanine-DNA methyltransferase (MGMT) promoter.
79 nation in the disposition of the inactivated O6-methylguanine-DNA methyltransferase (MGMT) protein in
82 ut suppressed methylation at the promoter of O6-methylguanine-DNA methyltransferase (MGMT) to enhance
88 rivatives is countered by the repair protein O6-methylguanine-DNA methyltransferase (MGMT), which rem
92 essor gene p16 (CDKN2A), the DNA repair gene O6-methylguanine-DNA-methyltransferase (MGMT) and the pu
94 r of metalloproteinase 3 (TIMP-3), p16INK4a, O6-methylguanine-DNA-methyltransferase (MGMT), death-ass
96 uced cells in vivo, selection based on P140K O6-methylguanine-DNA-methyltransferase (MGMT[P140K]) gen
97 yposis coli, APC; mut-L homolog 1, MLH1; and O(6)-methylguanine-DNA methyltransferase, MGMT) by liqui
98 vels of MET ligand hepatocyte growth factor, O(6)-methylguanine-DNA methyltransferase promoter methyl
99 TV a prolonged OS (P = 0.005) independent of O(6)-methylguanine-DNA-methyltransferase promoter methyl
100 ariate analysis, the factors age, WHO grade, O6-methylguanine-DNA methyltransferase promoter methylat
101 ed glioblastoma that harbors a nonmethylated O(6)-methylguanine-DNA methyltransferase promotor, stand
102 D-54 tumors, which do not express measurable O(6)-methylguanine-DNA methyltransferase protein, is pro
103 id anchors capable of covalent attachment to O(6)-methylguanine DNA methyltransferase (SNAP-tag) fusi
104 wed prognostic significance, with WHO grade, O6-methylguanine-DNA methyltransferase status, age, and
105 some methylated bases from DNA, and suicidal O(6)-methylguanine-DNA methyltransferases to transfer al
107 been identified in GBMs, except for loss of O(6-)methylguanine-DNA methyltransferase via promoter me
108 The percentage of patients methylated at O(6)-methylguanine-DNA methyltransferase was lower than