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1 s abolished by the denaturants triton X-100, Gua-HCl, Gua-thiocyanate, SDS and urea in a dose-depende
2 ns (X(2-) = FPO3(2-), HPO3(2-), or SO4(2-)), Gua(+) and GA into a functioning catalyst of the reducti
3 anine derived from BP (6-BP-8-Ade and 6-BP-8-Gua) and DBC (10-DBC-8-Ade and 10-DBC-8-Gua) were synthe
5 of the SM alpha-actin CArGs (both contain a Gua or Cyt substitution in their A/T-rich center) and th
6 the Gly136-Arg147 peptide cross-linked to a Gua at the N7 position, with the site of reaction being
7 n frequency of the three guanine C8 adducts, Gua-C8-AP, Gua-C8-1,6-ANP, and Gua-C8-1,8-ANP in a CGCG*
9 1-amino-6 ()-nitropyrene (Gua-C8-1,6-ANP and Gua-C8-1,8-ANP), which contain a nitro group on the pyre
11 ymerase iota complexed with N2-ethyl-Gua and Gua at the active site suggests movements in the DNA pol
12 NA polymerase iota opposite N2-ethyl-Gua and Gua using Mn2+ is lower relative to that using Mg2+ indi
15 ble for the observed selectivity against any Gua-containing basepair; 3) the Pro and Leu residues can
16 of the three guanine C8 adducts, Gua-C8-AP, Gua-C8-1,6-ANP, and Gua-C8-1,8-ANP in a CGCG*CG sequence
17 s with additional isosteric modifications at Gua and filter binding experiments revealed that the mec
19 s mutant enzyme by added guanidinium cation (Gua(+)): 1 M Gua(+) stabilizes the transition state by c
21 the enzyme pieces, (DeltaGS(double dagger))E+Gua = 2.4 kcal/mol, for Gua(+) activation of the R269A h
22 + HPi) pieces, (DeltaGS(double dagger))HPi+E+Gua = 5.6 kcal/mol, is nearly equal to the sum of the ad
24 (2)-epsilon-Gua and heptanone-1,N(2)-epsilon-Gua were substrates for enzymatic oxidation in rat liver
25 ucts [1,N(2)-epsilon-guanine (1,N(2)-epsilon-Gua), N(2),3-epsilon-Gua, heptanone-1,N(2)-epsilon-Gua,
26 N(2),3-epsilon-Gua, heptanone-1,N(2)-epsilon-Gua, 1,N(6)-epsilon-adenine (1,N(6)-epsilon-Ade), and 3,
27 guanine (1,N(2)-epsilon-Gua), N(2),3-epsilon-Gua, heptanone-1,N(2)-epsilon-Gua, 1,N(6)-epsilon-adenin
28 mber of differences between the 1,N2-epsilon-Gua and HO-ethanoGua adducts (which formally differ only
30 dGTP and dATP across from both 1,N2-epsilon-Gua and HO-ethanoGua, with the extent varying considerab
33 ated etheno ring derivative of 1, N2-epsilon-Gua, 5,6,7,9-tetrahydro-9-oxoimidazo[1,2-a]purine (ethan
34 ally the hydrated derivative of 1,N2-epsilon-Gua, is a stable DNA product also derived from vinyl hal
37 DNA polymerase iota complexed with N2-ethyl-Gua and Gua at the active site suggests movements in the
38 ion by DNA polymerase iota opposite N2-ethyl-Gua and Gua using Mn2+ is lower relative to that using M
39 ase iota incorporates dCMP opposite N2-ethyl-Gua and unadducted Gua with similar efficiencies in the
40 ructure of DNA polymerase iota with N2-ethyl-Gua at the active site reveals the adducted base in the
41 ncorporation and extension opposite N2-ethyl-Gua by DNA polymerase iota was measured and structures o
43 ity of DNA polymerase iota opposite N2-ethyl-Gua was determined by steady state kinetic analysis with
44 NA polymerase iota extends from the N2-ethyl-Gua:Cyt 3' terminus more efficiently than from the Gua:C
46 nd 22 microM for insertion of dTTP following Gua.C, 8-oxoGua.C, and 8-oxoGua.A base pairs, respective
47 aGS(double dagger))E+Gua = 2.4 kcal/mol, for Gua(+) activation of the R269A hlGPDH-catalyzed reaction
48 monstration that MMR specifically detects FU:Gua (in the first round of DNA replication), signaling a
50 mic DNA detected a mis-sense mutation (Ade-->Gua) that substitutes a conserved histidine at amino aci
51 pective bases hypoxanthine (Hx) and guanine (Gua) and the phosphoribosyl donor 5-phosphoribosyl-1-pyr
52 (Fapy) lesions of adenine (Ade) and guanine (Gua) to elucidate radical (.OH)-induced changes in DNA o
54 36-mer DNA duplex containing either guanine (Gua).C, 8-oxoGua.C, or 8-oxoGua.A base pairs at the prim
56 ed by the denaturants triton X-100, Gua-HCl, Gua-thiocyanate, SDS and urea in a dose-dependent manner
57 moethane-induced mutagenicity, one involving Gua N7-alkylation by alkyltransferase-S-CH2CH2Br and dep
59 me by added guanidinium cation (Gua(+)): 1 M Gua(+) stabilizes the transition state by ca. 3 kcal/mol
60 age for connection of hlGPDH (R269A mutant + Gua(+)) and substrate pieces (GA + HPi) pieces, (DeltaGS
61 )-guanyl)-9-hydroxyaflatoxin B(1) (AFB(1)-N7-Gua), which is converted naturally to two secondary lesi
62 mately 6 times higher than that of AFB(1)-N7-Gua, and (ii) one proposed rotamer of AFB(1)-FAPY is a b
65 zation procedures indicated that the AFB1-N7-Gua genome was approximately 95% pure with a small (5%)
66 he mutational asymmetry observed for AFB1-N7-Gua is consistent with structural models indicating that
69 8-(N7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N7-Gua) adduct was inserted into the single-stranded genome
70 - (N7-guanyl)-9-hydroxyaflatoxin B1 (AFB1-N7-Gua) adduct, the major DNA adduct of the potent liver ca
71 erty of the primary AFB1-DNA adduct, AFB1-N7-Gua, in mammalian cells has not been studied extensively
73 of AFB1-N7-Gua, unlike those (if the AFB1-N7-Gua-derived apurinic site, were much more strongly depen
75 r the conditions of the assay, the 4-OHE2-N7-Gua adduct (Km, 4.6+/-0.7 micromol/L; kcat, 45+/-1.6/h)
76 ydroxyestradiol-quinone to produce 4-OHE2-N7-Gua and 4-OHE2-N3-Ade in a time- and concentration-depen
77 4-OHE(2)-1(alpha,beta)-N7-guanine (4-OHE2-N7-Gua) and 4-OHE(2)-1(alpha,beta)-N3-adenine (4-OHE2-N3-Ad
78 s, N-(guanin-8-yl)-1-amino-6 ()-nitropyrene (Gua-C8-1,6-ANP and Gua-C8-1,8-ANP), which contain a nitr
79 This stabilization is due to the binding of Gua(+) to the binary E(mut) x OMP complex, with a K(d) o
81 nificant change in background levels of 8-OH-Gua and 8-OH-Ade was observed in control human cells, in
84 olysates should not generate additional 8-OH-Gua because of the absence of guanine, which is not rele
86 oreover, the Ntg1 protein releases free 8-OH-Gua from 8-OH-Gua/Gua duplex but not from duplexes conta
88 ce artifacts by oxidation of guanine to 8-OH-Gua in acid-hydrolysates of DNA, although the extent of
90 .6-fold (P < .02), whereas no change in 8-OH-Gua levels was observed in peripheral blood mononuclear
94 34mer DNA duplexes containing a single 8-OH-Gua residue mispaired with each of the four DNA bases.
95 erent stable-isotope labeled analogs of 8-OH-Gua used as internal standards for GC/IDMS analysis yiel
97 e results showed that 8-hydroxyguanine (8-OH-Gua) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (Fa
98 role in the repair of 8-hydroxyguanine (8-OH-Gua) in transcription-coupled and non-strand discriminat
100 midine (FapyAde), and 8-hydroxyguanine (8-OH-Gua) was observed among 17 lesions detected in damaged D
101 or example, mutagenic 8-hydroxyguanine (8-OH-Gua) was reduced approximately 50% (P = 0.02) in mice fe
102 efficient excision of 8-hydroxyguanine (8-OH-Gua), 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyG
107 e findings suggest that, in addition to 8-OH-Gua, FapyGua and FapyAde may be primary substrates for t
108 e findings suggest that, in addition to 8-OH-Gua, FapyGua may also be a primary substrate of yOgg1 in
109 g that NAC lowered the concentration of 8-OH-Gua, the log ratio, and the variance (previously associa
111 ates of D. radiodurans Fpg protein over 8-OH-Gua, whereas E. coli Fpg protein excises these three les
112 ted by the observation that incision of 8-OH-Gua- or 8-OH-Ade-containing oligodeoxynucleotides by who
116 tg1 protein releases free 8-OH-Gua from 8-OH-Gua/Gua duplex but not from duplexes containing 8-OH-Gua
118 ) for the addition of C opposite 8-oxoGua or Gua by KF- and pol II- were all biphasic, with a rapid i
120 ine glycosylase (hOGG1), which excises 8-oxo-Gua, strand breaks dependent upon this lesion were measu
122 uced by 1,2-dibromoethane were predominantly Gua to Ade transitions but, in the spectrum of such rifa
123 ic form of the complexes cis-[Pt(NH3)2(Am)(R-Gua)](2+), where R-Gua is 9-methyl- or 9-ethylguanine, i
124 lexes cis-[Pt(NH3)2(Am)(R-Gua)](2+), where R-Gua is 9-methyl- or 9-ethylguanine, is preferred over th
125 at adenine, the molecules designed to target Gua/Cyt sequences also generate lesions at guanine; howe
126 s obtained for DNA adducts other than at the Gua N7 atom and for mutations other than those attributa
131 es dCMP opposite N2-ethyl-Gua and unadducted Gua with similar efficiencies in the presence of Mg2+ an
132 et RNA-binding platform, which mimics 5'-Ura-Gua-3' by making Watson-Crick-like hydrogen bonds with 5
136 substrate, a 275-fold decrease in kcat with Gua, and a 500-fold decrease in kcat for IMP pyrophospho
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