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1 adenine and guanine derived from BP (6-BP-8-Ade and 6-BP-8-Gua) and DBC (10-DBC-8-Ade and 10-DBC-8-G
2 6-BP-8-Ade and 6-BP-8-Gua) and DBC (10-DBC-8-Ade and 10-DBC-8-Gua) were synthesized in good yields by
4 rmamidopyrimidine (Fapy) lesions of adenine (Ade) and guanine (Gua) to elucidate radical (.OH)-induce
8 logues resulted in release of Cl- or Br- and Ade, as well as partial reduction of E-NAD+ to E-NADH.
9 re was exploited by using the antiadenosine (Ade)-DNA aptamer (Apt-A) as a model functional nucleic a
11 ta-adenosine > 9-(cyclopentyl)-adenine (9-CP-Ade) >/= 9-(tetrahydrofuryl)-adenine (9-THF-Ade; SQ 22,5
14 resembles a molecular vise, with 5'-Ura-Cyt-Ade-Cyt-3' pinioned between an invariant Gly-X-X-Gly mot
16 -Gua, 1,N(6)-epsilon-adenine (1,N(6)-epsilon-Ade), and 3,N(4)-epsilon-cytosine (3,N(4)-epsilon-Cyt)]
17 vitro studies showed that both F-dAdo and F-Ade exert strong inhibition of T. vaginalis growth with
19 n (lethal event) or (b) depurination to form Ade and hexose-derived 6-carboxyl fluoride (HDCF), which
21 c electropolymerization from solution of FU, Ade-BTM, and tris([2,2'-bithiophen]-5-yl)methane (TTM) c
26 f genomic DNA detected a mis-sense mutation (Ade-->Gua) that substitutes a conserved histidine at ami
27 .5 times more efficiently than the 4-OHE2-N3-Ade adduct (Km, 4.6+/-1.0 micromol/L; kcat, 30+/-1.5/h).
30 resulting from direct conjugate addition of Ade to AF followed by hydrolytic cyclopropane ring-openi
31 of the bis(2,2'-bithienyl)methane moiety of Ade-BTM by the FU titrant, in benzonitrile, at 352 nm ex
32 ylated N(6) adenine, but in the presence of (Ade)2Cu complex the reaction mixture generated mono-, di
34 otein contributes to cellular repair of 8-OH-Ade and that the motif VI of the putative helicase domai
35 ge in background levels of 8-OH-Gua and 8-OH-Ade was observed in control human cells, indicating thei
36 in cellular repair of 8-hydroxyadenine (8-OH-Ade), another abundant lesion in oxidatively damaged DNA
38 servation that incision of 8-OH-Gua- or 8-OH-Ade-containing oligodeoxynucleotides by whole cell extra
40 oxy]phenyl-4-[bis(2,2'-bithienyl)methane] or Ade-BTM, was designed and synthesized for recognition of
42 ouble-stranded base pairs, Cyt/Oxa, Thy/Oxa, Ade/Oxa, and Gua/Oxa, with no preference to base pairing
48 of cytokinin-related genes revealed that Phe-Ade treatment established a typical cytokinin response.
50 (N)-A8 dihedral angle is 1.9 degrees and the Ade is virtually perpendicular to the corrin ring; in th
51 the corrin ring; in the minor conformer, the Ade is tilted down, and this dihedral is -48.7 degrees.
52 ptimal tracer candidate was selected for the Ade assay under buffer and realistic (diluted human seru
56 tion of the folded tertiary structure of the Ade-Apt-A complex triggered the release of the labeled n
58 an arc from over C15 to over C12, while the Ade ring oscillates from perpendicular to parallel to th
59 -Ade) >/= 9-(tetrahydrofuryl)-adenine (9-THF-Ade; SQ 22,536), with the exception of Type II adenylyl
60 ce human cells do not readily convert Ado to Ade, an understanding of the substrate preferences of th
61 1,2-dibromoethane were predominantly Gua to Ade transitions but, in the spectrum of such rifampicin-
62 me x anti-Adenosine with Asp40-COO- [E(40) x Ade(a)], Enzyme x syn-Adenosine with Asp40-COOH [E(40H)
63 yme x syn-Adenosine with Asp40-COO- [E(40) x Ade(s)], and Enzyme x anti-Inosine with Asp40-COO- [E(40
65 e x anti-Adenosine with Asp40-COOH [E(40H) x Ade(a)], Enzyme x anti-Adenosine with Asp40-COO- [E(40)
66 generated from the MD simulation of E(40H) x Ade(s) preserve the catalytically important hydrogen bon
68 me x syn-Adenosine with Asp40-COOH [E(40H) x Ade(s)], Enzyme x syn-Adenosine with Asp40-COO- [E(40) x
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