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