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1 mage by a suicide protein, O(6)-alkylguanine-DNA alkyltransferase.
2 nt in the DNA repair protein O6-alkylguanine-DNA alkyltransferase.
3 pathways devoted to their repair, including DNA alkyltransferases.
4 (PR) xenografts displayed no O6-alkylguanine-DNA alkyltransferase activity, and their levels of gluta
5 roportional to inhibition of O6-alkylguanine-DNA alkyltransferase activity, but a maximum tolerated d
6 mster ovary (CHO) cells lack O6-alkylguanine-DNA alkyltransferase (AGT) activity and are sensitive to
7 ls of the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT) and are sensitive to 1,3-bis(
8 cancer chemotherapy target O(6)-alkylguanine-DNA alkyltransferase (AGT) and paradoxically protect cel
9 hough it is known that (i) O(6)-alkylguanine-DNA alkyltransferase (AGT) confers tumor cell resistance
10 (MGMT), also referred to as O6-alkylguanine-DNA alkyltransferase (AGT) correlate with the resistance
11 ding the DNA repair enzyme O(6)-alkylguanine DNA alkyltransferase (AGT) from the O(6)-methylguanine m
23 of the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) is an important source of tum
24 ous infusion that suppresses O6-alkylguanine-DNA alkyltransferase (AGT) levels in brain tumors, (2) e
27 of the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) paradoxically increases the m
39 -inactive mutants of human O(6)-alkylguanine DNA alkyltransferase (AGT) show that it forms an O(6)-me
41 sistance via production of O(6)-alkylguanine DNA alkyltransferase (AGT) thereby enabling yd T cell fu
42 ss-link the repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT) to the N6 position of deoxyad
43 in oligonucleotides by human O6-alkylguanine DNA alkyltransferase (AGT) were estimated using rapid re
44 inal active site domain of O(6)-alkylguanine-DNA alkyltransferase (AGT) with an endonuclease V domain
45 he human DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), by O6-benzylguanine renders
48 r of the DNA repair protein, O6-alkylguanine-DNA alkyltransferase (AGT), has been shown to reduce nit
50 of the resistance protein O(6)-alkylguanine-DNA alkyltransferase (AGT), were synthesized and evaluat
51 chemical regulation of human O6-alkylguanine-DNA alkyltransferase (AGT), which determines the suscept
53 py is the DNA repair protein O6-alkylguanine-DNA alkyltransferase (AGT), which removes chlorethylatio
54 ves the DNA repair protein O(6)-alkylguanine-DNA alkyltransferase (AGT), which removes chloroethylati
55 resistance to expression of O6-alkylguanine-DNA alkyltransferase (AGT), which repairs DNA damage cau
56 In cells containing active O(6)-alkylguanine-DNA alkyltransferase (AGT), which repairs O(6)-meG, 3% m
57 trosamines are repaired by O(6)-alkylguanine DNA alkyltransferase (AGT), which transfers the O(6)-alk
58 an be directly repaired by O(6)-alkylguanine-DNA alkyltransferase (AGT), which transfers the pyridylo
59 sensitive factor (NSF) and O(6)-alklyguanine-DNA alkyltransferase (AGT), with moderate affinity (K ap
60 the involvement of BRCA2 in O6-alkylguanine DNA alkyltransferase (AGT)-mediated repair of O6-methylg
61 ficacy end point for overcoming alkylguanine DNA alkyltransferase (AGT)-mediated tumor cell resistanc
72 e marrow showed BG-resistant O6-alkylguanine-DNA-alkyltransferase (AGT) activity, and CFUs were stain
73 on of the DNA repair protein O6-alkylguanine-DNA-alkyltransferase (AGT) and increases rates of both s
74 The DNA repair protein O(6)-alkylguanine DNA-alkyltransferase (AGT) is known to form DNA cross-li
75 repair proteins related to O(6)-alkylguanine-DNA alkyltransferases (AGTs) that tightly bind alkylated
76 the human DNA repair protein O6-alkylguanine-DNA alkyltransferase (alkyltransferase) in vitro than O6
78 active as inactivators of O(6)-alkylguanine-DNA alkyltransferase (alkyltransferase) than either O(6)
81 ne (O6-BeG) on the levels of O6-alkylguanine-DNA alkyltransferase (ATase) in the hematopoietic compar
87 rreversible inactivator of O(6)-alkylguanine-DNA alkyltransferase currently in clinical trials to ove
88 ort here in vitro and in vivo studies on the DNA alkyltransferase from the thermophilic archaeon Sulf
89 a polymorphism in the human O6-alkylguanine-DNA alkyltransferase gene exists, with about 15% of the
90 study of recombinant human O(6)-alkylguanine-DNA alkyltransferase (hAGT) revealed a previously unknow
91 ive site cysteine of human O(6)-alkylguanine-DNA alkyltransferase (hAGT), Cys145, was shown to be hig
92 xpression of human protein O(6)-alkylguanine-DNA alkyltransferase (hAGT), in which the active site cy
93 el of the DNA repair protein O6-alkylguanine-DNA alkyltransferase in brain tumors was correlated with
94 that the DNA repair protein O6-alkylguanine-DNA alkyltransferase increases the mutagenicity of 1,2-d
95 y lower in the cells lacking O6-alkylguanine-DNA alkyltransferase, indicating that O6-MeG was causall
96 carmustine (BCNU) plus the O(6)-alkylguanine-DNA alkyltransferase inhibitor O(6)-benzylguanine (O(6)-
98 uanine (BG), an inhibitor of O6-alkylguanine-DNA alkyltransferase, is being tested clinically for its
99 an chorionic gonadotropin-O(6) -alkylguanine-DNA alkyltransferase) led to LAMP-to-hCG signal transduc
101 Epigenetic regulation of O(6)-alkylguanine DNA alkyltransferase (MGMT) is surrogate of intrinsic re
104 ducts in DNA are repaired by O6-alkylguanine-DNA alkyltransferases (MGMT) by transfer of the alkyl gr
105 stem cell function include O(6)-alkylguanine DNA alkyltransferase, nucleotide excision repair, base e
106 d the translocation of the O(6)-alkylguanine DNA alkyltransferase on DNA, reaching single base-pair r
109 e DNA repair protein human O(6)-alkylguanine-DNA alkyltransferase repairs lesions at the 5' ends of 7
111 , differing only in level of O6-alkylguanine-DNA alkyltransferase, were treated with MNU and assayed
112 s of the DNA repair protein, O6-alkylguanine-DNA alkyltransferase, which may explain their susceptibi