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1 s and a potent pre-mutagenic lesion prone to mispair with 2'-deoxyadenosine (dA).
2  that catalyzes the removal of adenine bases mispaired with 2'-deoxyguanosine and 7,8-dihydro-8-oxo-2
3 Y from Escherchia coli is removal of adenine mispaired with 7,8-dihydro-8-oxoguanine (8-oxoG), a comm
4     One of these enzymes, MutY, excises an A mispaired with 8-oxoG as part of the process to restore
5 h G, C or 8-oxoG and weakly removing guanine mispaired with 8-oxoG.
6  MutY homolog-dependent excision of adenines mispaired with 8-oxoguanine (G(O)) also act as MMR initi
7 lly cleaves a DNA duplex containing 8-OH-Gua mispaired with a guanine.
8 Y has high binding affinity with 8-oxoG when mispaired with A, G, T, C, or inosine.
9  spiroiminodihydantoin (Sp) because of their mispairing with A or G.
10  G418 increases functional near-cognate tRNA mispairing with a PSC, resulting from binding to its tig
11 tive oxygen species, is mutagenic because it mispairs with A.
12 oG) is a dangerous DNA lesion because it can mispair with adenine (A) during replication resulting in
13 oguanine (oxoG), an abundant DNA lesion, can mispair with adenine and induce mutations.
14                           Because 8-oxoG can mispair with adenine during DNA synthesis, it is of inte
15 ex but not from duplexes containing 8-OH-Gua mispaired with adenine, thymine or cytosine.
16 e damage is 8-oxo-2'-deoxyguanosine (8-oxoG) mispairing with adenine (Ade), which can occur in two wa
17                                           By mispairing with adenine during replication, oxoG gives r
18  DNA polymerases, is highly mutagenic due to mispairing with adenine.
19 ich is highly mutagenic as it preferentially mispairs with adenine (A) during replication.
20 ely damaged guanines [8-oxoguanine (8-oxoG)] mispaired with adenines (8-oxoG.A).
21 easurements of the quantum yield of 8-DEA-tC mispaired with adenosine and, separately, opposite an ab
22 ity of PolB1 was the highest when 8-oxoG was mispaired with an incorrect nucleotide and could therefo
23 does not incise duplexes containing 8-OH-Gua mispaired with any of the four DNA bases.
24 oximately 17-fold more efficiently than when mispaired with dA, which is misinserted by DNA polymeras
25 s high mutagenic potential as it is prone to mispair with deoxyadenine (dA).
26 ycol (Tg), 5,6-dihydroxy-5,6-dihydrothymine, mispaired with deoxyguanosine.
27 uplexes containing a single 8-OH-Gua residue mispaired with each of the four DNA bases.
28 on of genomic DNA because 8-oxoG can readily mispair with either cytosine or adenine.
29                    By contrast, dsTCR chains mispaired with endogenous chains cannot properly assembl
30 ed DNA glycosylase activity removing adenine mispaired with G, C or 8-oxoG and weakly removing guanin
31 rent sequence contexts and when present in a mispair with guanine.
32 mU-DNA glycosylase activity that removes HmU mispaired with guanine has been measured.
33 as the base 5-fluorouracil (FU) in DNA) when mispaired with guanine, but not paired with adenine.
34 nd and when correctly paired with adenine or mispaired with guanine.
35  further confirmed using 5-fluorouracil (FU) mispaired with guanine.
36 dified uracils (e.g., 5-hydroxymethyluracil) mispaired with guanine.
37 tes include either uracil or thymine adducts mispaired with guanine.
38           Because the thymine analog 5-BrUra mispairs with guanine in DNA, generation of brominated p
39 sion of 8-oxoguanine from thermally unstable mispairs with guanine or thymine, while excision from th
40 e that removes adenines or 2-hydroxyadenines mispaired with guanines or 8-oxoguanines.
41 ota generates a variety of single and tandem mispairs with high frequency, implying that it may act a
42 2, +4, and +10 insertion/deletion loop (IDL) mispairs with K(d) values of 0.20, 0.25, 11, 3.2, and 0.
43  to perfectly match wildtype sequences while mispairing with mutants, long blockers enable 14-44 nt e
44 onably stable and strongly selective against mispairing with native bases.
45                      These two adducts, when mispaired with normal bases, were all excised from DNA b
46 e mismatch repair complex MSH2-MSH6 binds to mispairs with only slightly higher affinity than to full
47            The tight binding of MutY with GO mispaired with T, G, and apurinic/apyrimidinic sites may
48 emains closed in single-stranded DNA or when mispaired with T.
49 closed state is achieved for the A*G and G*G mispair with the incoming dGTP in anti conformation, whi
50 guingly, the simulations reveal that the G*G mispair with the incoming nucleotide in the syn configur
51 mplating base, thereby competing against the mispairing with the templating base.
52 esentative oxidative DNA lesions, frequently mispairs with the incoming dAMP during mammalian DNA rep
53 t unrepaired O(6)-methyldeoxyguanine lesions mispaired with thymine during the first replication cycl
54                             O6-methylguanine mispairs with thymine during replication, and if the add
55  TMZ produces O6-methylguanine in DNA, which mispairs with thymine during the next cycle of DNA repli
56 ces O(6)-methylguanine in DNA, which in turn mispairs with thymine, triggering futile DNA mismatch re
57 e-specific differences were observed for one mispair, with WT RT preferentially resolving dC-rC pairs