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1 epair by direct dealkylation of mutagenic O6-alkylguanine.
2 ollowing exposure to alkylating agents is O6-alkylguanine.
3 at DNA-carcinogen adducts, specifically O(6)-alkylguanine.
4 s in the G:C to A:T mutations caused by O(6)-alkylguanine.
5 igodeoxyribonucleotides (ODNs) containing O6-alkylguanines.
6 , suggesting that the observed decline in O6-alkylguanine adduct yields is, at least partially, a res
7 ects S.pombe against the toxic effects of O6-alkylguanine adducts and the biological function of a fa
8 of PAH diol epoxides, NNK-induced N7- and O6-alkylguanine adducts are not preferentially formed at th
13 g novel AGT inhibitors that incorporate O(6)-alkylguanine adducts in oligodeoxyribonucleotide context
14 ENZI: TP opposite biologically relevant O(6)-alkylguanine adducts is characterized herein as a basis
15 erapeutic effectiveness of agents forming O6-alkylguanine adducts such as BCNU might be enhanced.
16 f simple alkylating agents by repairing O(6)-alkylguanine adducts via a direct transfer reaction.
20 the gene coding for a mutant version of O(6)-alkylguanine alkyltransferase, which is efficiently asse
21 ation of Atl1 from DNA containing small O(6)-alkylguanines allows accurate completion of global genom
22 ty than TTHA1564 to distinguish between O(6)-alkylguanine and guanine and in an unprecedented mechani
25 alkyltransferase (AGT) repairs mutagenic O6-alkylguanine and O4-alkylthymine adducts in single-stran
26 uanine-DNA alkyltransferase (AGT) repairs O6-alkylguanine and O4-alkylthymine adducts in single-stran
27 d have no activity toward other, less stable alkylguanines as previously described for YtkR2/AlkD and
28 the electrostatic potential surface of O(6)-alkylguanine, as determined using molecular mechanics ca
29 d, in comparison with the corresponding O(6)-alkylguanines, as potential inhibitors of the DNA-repair
30 the cysteine acceptor site (Cys145), the O6-alkylguanine binding pocket, and a DNA binding domain.
31 ), whereas strong Atl1 binding to bulky O(6)-alkylguanines blocks GGR, stalls the transcription machi
33 the PB2 cap-binding domain suggested that 7-alkylguanine derivatives substituted at position N-9 and
34 to oligodeoxyribonucleotides containing O(6)-alkylguanines differing in size, polarity, and charge of
35 f the artificial nucleotide opposite an O(6)-alkylguanine DNA adduct was verified using a novel 2',3'
36 ly with sensitivity to agents that form O(6)-alkylguanine DNA adducts, such as carmustine (BCNU), tem
37 l vector encoding the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT) from the O(6)-me
41 r-active and -inactive mutants of human O(6)-alkylguanine DNA alkyltransferase (AGT) show that it for
42 onfers TMZ resistance via production of O(6)-alkylguanine DNA alkyltransferase (AGT) thereby enabling
43 (Bz) guanine in oligonucleotides by human O6-alkylguanine DNA alkyltransferase (AGT) were estimated u
45 o-specific nitrosamines are repaired by O(6)-alkylguanine DNA alkyltransferase (AGT), which transfers
46 , we describe the involvement of BRCA2 in O6-alkylguanine DNA alkyltransferase (AGT)-mediated repair
47 iochemical efficacy end point for overcoming alkylguanine DNA alkyltransferase (AGT)-mediated tumor c
51 ly mutagenic, and it can be repaired by O(6)-alkylguanine DNA alkyltransferase and mismatch repair pa
52 n, we observed the translocation of the O(6)-alkylguanine DNA alkyltransferase on DNA, reaching singl
53 r defects on stem cell function include O(6)-alkylguanine DNA alkyltransferase, nucleotide excision r
54 RI, and further clinical data, such as O (6)-alkylguanine DNA methyltransferase (MGMT) and telomerase
57 nt inactivator of the DNA-repair protein, O6-alkylguanine-DNA alkyl-transferase (AGT), that enhances
58 Chinese hamster ovary (CHO) cells lack O6-alkylguanine-DNA alkyltransferase (AGT) activity and are
59 ress low levels of the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) and are sensitiv
60 ifs with the cancer chemotherapy target O(6)-alkylguanine-DNA alkyltransferase (AGT) and paradoxicall
62 yltransferase (MGMT), also referred to as O6-alkylguanine-DNA alkyltransferase (AGT) correlate with t
73 as a continuous infusion that suppresses O6-alkylguanine-DNA alkyltransferase (AGT) levels in brain
75 The presence of the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) paradoxically in
87 that can cross-link the repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) to the N6 positi
88 of the C-terminal active site domain of O(6)-alkylguanine-DNA alkyltransferase (AGT) with an endonucl
89 tivation of the human DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), by O6-benzylgua
90 tent inhibitor of the DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), has been shown
92 an inhibitor of the resistance protein O(6)-alkylguanine-DNA alkyltransferase (AGT), were synthesize
95 therapy involves the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT), which removes c
96 osourea therapy is the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT), which removes c
97 nship of this resistance to expression of O6-alkylguanine-DNA alkyltransferase (AGT), which repairs D
99 O(6)-POB-dG can be directly repaired by O(6)-alkylguanine-DNA alkyltransferase (AGT), which transfers
107 arious ethylene crosslinks of DNA with O(6) -alkylguanine-DNA alkyltransferase (AGT, see picture).
108 ctivators of the human DNA repair protein O6-alkylguanine-DNA alkyltransferase (alkyltransferase) in
110 200-fold less active as inactivators of O(6)-alkylguanine-DNA alkyltransferase (alkyltransferase) tha
111 6-benzylguanine (O6-BeG) on the levels of O6-alkylguanine-DNA alkyltransferase (ATase) in the hematop
113 tallographic study of recombinant human O(6)-alkylguanine-DNA alkyltransferase (hAGT) revealed a prev
115 ablished by expression of human protein O(6)-alkylguanine-DNA alkyltransferase (hAGT), in which the a
119 and D-245 MG (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their le
120 l responses proportional to inhibition of O6-alkylguanine-DNA alkyltransferase activity, but a maximu
122 anine is an irreversible inactivator of O(6)-alkylguanine-DNA alkyltransferase currently in clinical
123 recently that a polymorphism in the human O6-alkylguanine-DNA alkyltransferase gene exists, with abou
124 that the level of the DNA repair protein O6-alkylguanine-DNA alkyltransferase in brain tumors was co
125 been proposed that the DNA repair protein O6-alkylguanine-DNA alkyltransferase increases the mutageni
126 II trial of carmustine (BCNU) plus the O(6)-alkylguanine-DNA alkyltransferase inhibitor O(6)-benzylg
128 erved that the DNA repair protein human O(6)-alkylguanine-DNA alkyltransferase repairs lesions at the
129 protein (human chorionic gonadotropin-O(6) -alkylguanine-DNA alkyltransferase) led to LAMP-to-hCG si
130 significantly lower in the cells lacking O6-alkylguanine-DNA alkyltransferase, indicating that O6-Me
131 O6-benzylguanine (BG), an inhibitor of O6-alkylguanine-DNA alkyltransferase, is being tested clini
132 rain MISU-1.1, differing only in level of O6-alkylguanine-DNA alkyltransferase, were treated with MNU
133 ain low levels of the DNA repair protein, O6-alkylguanine-DNA alkyltransferase, which may explain the
136 class of DNA repair proteins related to O(6)-alkylguanine-DNA alkyltransferases (AGTs) that tightly b
137 kylguanine adducts in DNA are repaired by O6-alkylguanine-DNA alkyltransferases (MGMT) by transfer of
139 n and depletion of the DNA repair protein O6-alkylguanine-DNA-alkyltransferase (AGT) and increases ra
144 minal addition of SNAP or CLIP forms of O(6)-alkylguanine-DNA-alkyltransferase plus a peptide epitope
145 ubiquitous DNA repair protein, removes O(6)-alkylguanine from DNA, including cytotoxic O(6)-chloroet
146 s stoichiometrically the alkyl group from O6-alkylguanine in DNA at the Cys-321 residue and from alky
147 of N-nitrosamines depends on formation of O6-alkylguanine in DNA, the formation of the analog S6-meth
148 erminal domain of hAGT was able to repair O6-alkylguanine in vitro via alkyl transfer provided that z
149 ransfers the pyridyloxobutyl group from O(6)-alkylguanines in DNA to an active site cysteine residue
151 omer in removing the mutagenic DNA adduct O6-alkylguanine (induced by alkylating carcinogens) via a s
153 his suggests that Atl1 acts by binding to O6-alkylguanine lesions and signalling them for processing
154 Alkyltransferase-like enzymes mark O(6)-alkylguanine lesions and, depending on adduct size, chan
155 crease has been attributed to mutagenic O(6)-alkylguanine lesions being formed via the alkylation of
156 t in hepatitis-B cirrhosis, the repair of O6-alkylguanine lesions by ATase may be less efficient than
157 against the genotoxic effects of other O(6)-alkylguanine lesions by removing alkyl groups from the O
158 Among the various DNA lesions formed, O(6)-alkylguanine lesions can be highly cytotoxic, and we rec
160 ts of DNA alkylation damage by flagging O(6)-alkylguanine lesions for nucleotide excision repair (NER
161 e (MGMT) is the sole repair protein for O(6)-alkylguanine lesions in DNA and has been reported to be
163 cies are efficient in repairing genotoxic O6-alkylguanine lesions induced by methylating (streptozoto
164 MGMT) repairs the mutagenic and cytotoxic O6-alkylguanine lesions produced by environmental carcinoge
165 nd raise the question of whether or not O(6)-alkylguanine lesions that are poor substrates for the al
166 ltransferase (MGMT) dealkylates mutagenic O6-alkylguanine lesions within DNA in an irreversible react
168 s is due to decreased repair capacity for O6-alkylguanine, removal of this lesion from DNA was assess
169 or insertion of dCTP opposite a series of N2-alkylguanine templates of increasing size from (methyl (
170 ects from alkylating agents by converting O6-alkylguanine to guanine forming S-methylcysteine in the
171 the promutagenic and cytotoxic DNA lesion O6-alkylguanine, was examined by immunostaining in a series
172 protein, removes the mutagenic DNA adduct O6-alkylguanine, which is synthesized both endogenously and
173 HTH motif to stabilize the extrahelical O(6)-alkylguanine without the protein conformational change o