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1 by a suicide protein, O(6)-alkylguanine-DNA alkyltransferase.
2 n the DNA repair protein O6-alkylguanine-DNA alkyltransferase.
3 ay using monoclonal antibodies against human alkyltransferase.
4 tested for their ability to inactivate human alkyltransferase.
5 hways devoted to their repair, including DNA alkyltransferases.
6 ces the cysteine at the known active site of alkyltransferases.
7 an CblC exhibits glutathione (GSH)-dependent alkyltransferase activity and flavin-dependent reductive
12 xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of glutathio
13 rtional to inhibition of O6-alkylguanine-DNA alkyltransferase activity, but a maximum tolerated dose
18 r ovary (CHO) cells lack O6-alkylguanine-DNA alkyltransferase (AGT) activity and are sensitive to kil
19 rrow showed BG-resistant O6-alkylguanine-DNA-alkyltransferase (AGT) activity, and CFUs were stained i
20 f the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) and are sensitive to 1,3-bis(2-ch
21 f the DNA repair protein O6-alkylguanine-DNA-alkyltransferase (AGT) and increases rates of both spont
22 er chemotherapy target O(6)-alkylguanine-DNA alkyltransferase (AGT) and paradoxically protect cells f
23 h it is known that (i) O(6)-alkylguanine-DNA alkyltransferase (AGT) confers tumor cell resistance to
24 MT), also referred to as O6-alkylguanine-DNA alkyltransferase (AGT) correlate with the resistance of
25 the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT) from the O(6)-methylguanine methy
26 The DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) has been shown to protect cells f
27 To evaluate the role of O6-alkylguanine-DNA alkyltransferase (AGT) in colon tumor chloroethylnitroso
37 the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) is an important source of tumor c
38 The DNA repair protein O(6)-alkylguanine DNA-alkyltransferase (AGT) is known to form DNA cross-links
39 The DNA repair protein O(6)-alkylguanine alkyltransferase (AGT) is responsible for removing promu
40 infusion that suppresses O6-alkylguanine-DNA alkyltransferase (AGT) levels in brain tumors, (2) evalu
41 Another way to deplete O6-alkylguanine DNA alkyltransferase (AGT) levels is to modify methylating a
43 the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) paradoxically increases the mutag
47 The DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) protects cells from alkylation da
49 The repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) protects cells from the mutagenic
55 ctive mutants of human O(6)-alkylguanine DNA alkyltransferase (AGT) show that it forms an O(6)-methyl
57 ance via production of O(6)-alkylguanine DNA alkyltransferase (AGT) thereby enabling yd T cell functi
58 ity of O(6)-benzylguanine (BG) to inactivate alkyltransferase (AGT) to potentiate the antitumor effic
59 ink the repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) to the N6 position of deoxyadenos
60 ligonucleotides by human O6-alkylguanine DNA alkyltransferase (AGT) were estimated using rapid reacti
61 active site domain of O(6)-alkylguanine-DNA alkyltransferase (AGT) with an endonuclease V domain.
62 uman DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), by O6-benzylguanine renders tumo
63 The DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT), encoded by the gene MGMT, repair
65 the DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), has been shown to reduce nitroso
66 The DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), protects cells from the toxic an
67 the resistance protein O(6)-alkylguanine-DNA alkyltransferase (AGT), were synthesized and evaluated f
68 ical regulation of human O6-alkylguanine-DNA alkyltransferase (AGT), which determines the susceptibil
70 s the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT), which removes chlorethylation or
71 the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT), which removes chloroethylation o
72 istance to expression of O6-alkylguanine-DNA alkyltransferase (AGT), which repairs DNA damage caused
73 ells containing active O(6)-alkylguanine-DNA alkyltransferase (AGT), which repairs O(6)-meG, 3% misin
74 amines are repaired by O(6)-alkylguanine DNA alkyltransferase (AGT), which transfers the O(6)-alkyl g
75 e directly repaired by O(6)-alkylguanine-DNA alkyltransferase (AGT), which transfers the pyridyloxobu
76 itive factor (NSF) and O(6)-alklyguanine-DNA alkyltransferase (AGT), with moderate affinity (K approx
77 involvement of BRCA2 in O6-alkylguanine DNA alkyltransferase (AGT)-mediated repair of O6-methylguani
78 cy end point for overcoming alkylguanine DNA alkyltransferase (AGT)-mediated tumor cell resistance to
89 ir proteins related to O(6)-alkylguanine-DNA alkyltransferases (AGTs) that tightly bind alkylated DNA
90 human DNA repair protein O6-alkylguanine-DNA alkyltransferase (alkyltransferase) in vitro than O6-ben
92 ive as inactivators of O(6)-alkylguanine-DNA alkyltransferase (alkyltransferase) than either O(6)-ben
93 ctural conformations related to the distinct alkyltransferase and acetyltransferase reactions catalyz
94 than O6-benzylguanine against the wild-type alkyltransferase and is even capable of inactivating the
96 inding proteins, agt for an alkyl-cysteine-S-alkyltransferase and Taf1 for a subunit of transcription
97 ery slow, whereas the E. coli Ogt, the human alkyltransferase, and the mutant A316P/W336A-Ada-C alkyl
101 O6-BeG) on the levels of O6-alkylguanine-DNA alkyltransferase (ATase) in the hematopoietic compartmen
102 The DNA repair protein, O6-alkylguanine-DNA alkyltransferase (ATase) is an important cellular resist
106 ersible inactivator of O(6)-alkylguanine-DNA alkyltransferase currently in clinical trials to overcom
108 rary was selected for the ability to provide alkyltransferase-deficient Escherichia coli with resista
110 dence supports the existence of at least two alkyltransferase-dependent pathways for 1,2-dibromoethan
111 est that the enzyme belongs to the family of alkyltransferase enzymes for which Zn plays a key role i
112 est that the enzyme belongs to the family of alkyltransferase enzymes for which Zn plays a role in ac
113 here in vitro and in vivo studies on the DNA alkyltransferase from the thermophilic archaeon Sulfolob
114 olymorphism in the human O6-alkylguanine-DNA alkyltransferase gene exists, with about 15% of the popu
116 y of recombinant human O(6)-alkylguanine-DNA alkyltransferase (hAGT) revealed a previously unknown zi
117 site cysteine of human O(6)-alkylguanine-DNA alkyltransferase (hAGT), Cys145, was shown to be highly
118 ssion of human protein O(6)-alkylguanine-DNA alkyltransferase (hAGT), in which the active site cystei
119 f the DNA repair protein O6-alkylguanine-DNA alkyltransferase in brain tumors was correlated with res
122 rotein O6-alkylguanine-DNA alkyltransferase (alkyltransferase) in vitro than O6-benzylguanine, the pr
123 ise as an agent for possible tumor-selective alkyltransferase inactivation, which suggests it may pro
124 n vitro than O6-benzylguanine, the prototype alkyltransferase inactivator currently in clinical trial
125 provide a new class of highly water-soluble alkyltransferase inactivators and form the basis to cons
126 O6-benzyl-2'-deoxyguanosine were more potent alkyltransferase inactivators than the parent nucleoside
127 t the DNA repair protein O6-alkylguanine-DNA alkyltransferase increases the mutagenicity of 1,2-dibro
128 wer in the cells lacking O6-alkylguanine-DNA alkyltransferase, indicating that O6-MeG was causally in
130 ustine (BCNU) plus the O(6)-alkylguanine-DNA alkyltransferase inhibitor O(6)-benzylguanine (O(6)-BG)
131 lguanine and that higher doses or additional alkyltransferase inhibitors capable of inactivating this
135 ne (BG), an inhibitor of O6-alkylguanine-DNA alkyltransferase, is being tested clinically for its abi
136 illing of tumors that express high levels of alkyltransferase, it would also be expected to reduce th
137 horionic gonadotropin-O(6) -alkylguanine-DNA alkyltransferase) led to LAMP-to-hCG signal transduction
138 ld encourage prospective studies to evaluate alkyltransferase levels as a method, for identifying bra
140 d also be expected to reduce the already low alkyltransferase levels of hematopoietic stem cells and,
146 reveal the presence of a group of proteins [alkyltransferase-like (ATL) proteins] showing amino acid
147 ccharomyces pombe a DNA recognition protein, alkyltransferase-like 1 (Atl1), can play a pivotal role
149 R process in those organisms that express an alkyltransferase-like gene and raise the question of whe
155 ase currently in clinical trials to overcome alkyltransferase-mediated resistance to certain cancer c
156 igenetic regulation of O(6)-alkylguanine DNA alkyltransferase (MGMT) is surrogate of intrinsic resist
160 s in DNA are repaired by O6-alkylguanine-DNA alkyltransferases (MGMT) by transfer of the alkyl group
161 D34+) hematopoietic precursors do not induce alkyltransferase, myelosuppression may be the dose-limit
162 cell function include O(6)-alkylguanine DNA alkyltransferase, nucleotide excision repair, base excis
164 e translocation of the O(6)-alkylguanine DNA alkyltransferase on DNA, reaching single base-pair resol
165 lamin intermediate via glutathione-dependent alkyltransferase or reductive elimination activities.
170 ine lesions that are poor substrates for the alkyltransferase proteins in higher eukaryotes might, by
172 olecular modeling of their interactions with alkyltransferase provided a molecular explanation for th
173 are better substrates than methyl groups for alkyltransferases provided that steric factors do not pr
175 ransferase, and the mutant A316P/W336A-Ada-C alkyltransferases reacted very rapidly with this 16-mer
176 previous proposal that AANAT can catalyze an alkyltransferase reaction in a conformationally altered
178 A repair protein human O(6)-alkylguanine-DNA alkyltransferase repairs lesions at the 5' ends of 70-nu
179 genicity, one involving Gua N7-alkylation by alkyltransferase-S-CH2CH2Br and depurination, plus anoth
181 e we report the X-ray structure of the human alkyltransferase solved using the technique of multiple
182 effective in preventing mutations than human alkyltransferase, suggesting that the endonuclease V act
183 s of O(6)-alkylguanine-DNA alkyltransferase (alkyltransferase) than either O(6)-benzylguanine or O(6)
184 ven capable of inactivating the P140K mutant alkyltransferase that is resistant to inactivation by O6
186 to interpret the behaviour of certain mutant alkyltransferases to enhance biochemical understanding o
187 d in epoxide carboxylation: a zinc-dependent alkyltransferase, two short-chain dehydrogenases with sp
188 e subpopulation of cells with high levels of alkyltransferase was correlated directly with drug resis
189 ffering only in level of O6-alkylguanine-DNA alkyltransferase, were treated with MNU and assayed for
190 ta-position greatly enhances inactivation of alkyltransferase, whereas para-substitution has little e
191 ng for a mutant version of O(6)-alkylguanine alkyltransferase, which is efficiently assembled with an
192 the DNA repair protein, O6-alkylguanine-DNA alkyltransferase, which may explain their susceptibility
194 cubation of Escherichia coli-expressed human alkyltransferase with 1,2-dibromoethane and single-stran
195 phan, or alanine on the interaction of human alkyltransferase with O6-benzylguanine using direct dete