ライフサイエンスコーパス: Ade

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

3 In addition, Ade and halide ions were released from the inhibitors in

4 rmamidopyrimidine (Fapy) lesions of adenine (Ade) and guanine (Gua) to elucidate radical (.OH)-induce

5 unobstructed Watson-Crick faces of adenine (Ade) pointing towards the MOF cavities.

6 r- and F- ions and the formation of adenine (Ade).

7 disorder in the orientation of the adenine (Ade) moiety relative to the ribose of the Ado ligand.

8 yguanosine (8-oxoG) mispairing with adenine (Ade), which can occur in two ways.

9 Adenosine (Ade) has been identified to stimulate bone formation.

10 mical synthesis of the corresponding 3-alkyl-Ade adduct.

11 logues resulted in release of Cl- or Br- and Ade, as well as partial reduction of E-NAD+ to E-NADH.

12 re was exploited by using the antiadenosine (Ade)-DNA aptamer (Apt-A) as a model functional nucleic a

13 arget DNA methylation in the minor groove at Ade/Thy- and/or Gua/Cyt-rich sequences.

14 ta-adenosine > 9-(cyclopentyl)-adenine (9-CP-Ade) >/= 9-(tetrahydrofuryl)-adenine (9-THF-Ade; SQ 22,5

15 ssentially insensitive to inhibition by 9-CP-Ade.

16 Watson-Crick-like hydrogen bonds with 5'-Cyt-Ade-3'.

17 resembles a molecular vise, with 5'-Ura-Cyt-Ade-Cyt-3' pinioned between an invariant Gly-X-X-Gly mot

18 subunit alpha (AtpA) and adenine deaminase (Ade, which catalyzes conversion of adenine to hypoxanthi

19 n-2-ylidene (Gua, Cyt), 2,4-dimethylbenzoyl (Ade, Cyt), and Bz (Thy)].

20 A human p53-driven Ade reporter system in yeast was used to study the facto

21 -Gua, 1,N(6)-epsilon-adenine (1,N(6)-epsilon-Ade), and 3,N(4)-epsilon-cytosine (3,N(4)-epsilon-Cyt)]

22 vitro studies showed that both F-dAdo and F-Ade exert strong inhibition of T. vaginalis growth with

23 releases highly cytotoxic 2-fluoroadenine (F-Ade).

24 n (lethal event) or (b) depurination to form Ade and hexose-derived 6-carboxyl fluoride (HDCF), which

25 ts reactivity in aqueous media with the free Ade base is more than 600 times that of CGenQ.

26 c electropolymerization from solution of FU, Ade-BTM, and tris([2,2'-bithiophen]-5-yl)methane (TTM) c

27 The stability constant of the FU-Ade-BTM complex of 1:2 stoichiometry was K = 2.17(+/-0.0

28 yl)methane (TTM) cross-linking monomer at FU:Ade-BTM:TTM = 1:2:3 mol ratio.

29 order of reaction determined was Gua>Thy>Cyt>Ade.

30 d into solution and chemically degrades into Ade, halide ion, and sugar-derived products.

31 epaired in time, DNA polymerases can mispair Ade with 8-oxoG in the template.

32 f genomic DNA detected a mis-sense mutation (Ade-->Gua) that substitutes a conserved histidine at ami

33 .5 times more efficiently than the 4-OHE2-N3-Ade adduct (Km, 4.6+/-1.0 micromol/L; kcat, 30+/-1.5/h).

34 inone to produce 4-OHE2-N7-Gua and 4-OHE2-N3-Ade in a time- and concentration-dependent manner.

35 4-OHE(2)-1(alpha,beta)-N3-adenine (4-OHE2-N3-Ade).

36 resulting from direct conjugate addition of Ade to AF followed by hydrolytic cyclopropane ring-openi

37 fects and enable the clinical application of Ade for treating large bone defects.

38 of the bis(2,2'-bithienyl)methane moiety of Ade-BTM by the FU titrant, in benzonitrile, at 352 nm ex

39 nanofibrous mats with 0.3:0.4 (w/w) ratio of Ade and PVA showed a sustained and controlled release of

40 showed a sustained and controlled release of Ade and facilitated the osteogenic differentiation of bo

41 However, the use of Ade is severely limited by the accompanying side effects

42 ylated N(6) adenine, but in the presence of (Ade)2Cu complex the reaction mixture generated mono-, di

43 d using the mathematical model log(10)[(8-OH-Ade + 8-OH-Gua)/(FapyAde + FapyGua)].

44 otein contributes to cellular repair of 8-OH-Ade and that the motif VI of the putative helicase domai

45 ge in background levels of 8-OH-Gua and 8-OH-Ade was observed in control human cells, indicating thei

46 in cellular repair of 8-hydroxyadenine (8-OH-Ade), another abundant lesion in oxidatively damaged DNA

47 ively modified lesion 8-hydroxyadenine (8-OH-Ade).

48 servation that incision of 8-OH-Gua- or 8-OH-Ade-containing oligodeoxynucleotides by whole cell extra

49 ogically important lesions 8-OH-Gua and 8-OH-Ade.

50 oxy]phenyl-4-[bis(2,2'-bithienyl)methane] or Ade-BTM, was designed and synthesized for recognition of

51 7-mer) positioned opposite Cyt, Gua, Thy, or Ade.

52 ouble-stranded base pairs, Cyt/Oxa, Thy/Oxa, Ade/Oxa, and Gua/Oxa, with no preference to base pairing

53 fabricated poly(epsilon-caprolactone) (PCL)/Ade-polyvinyl alcohol (PVA)((0.3/0.4)) nanofibrous mats

54 ed in vivo in the cranial defects of the PCL/Ade-PVA((0.3/0.4)) group compared with those of the non-

55 ound, the cytokinin-like phenyl-adenine (Phe-Ade), as a potent inducer of adventitious shoots.

56 Although Phe-Ade triggered diverse cytokinin-dependent phenotypical r

57 Collectively, Phe-Ade exhibits a dual mode of action that results in a str

58 Moreover, Phe-Ade activated the cytokinin receptors ARABIDOPSIS HISTID

59 In addition, we demonstrated that Phe-Ade is a strong competitive inhibitor of CYTOKININ OXIDA

60 of cytokinin-related genes revealed that Phe-Ade treatment established a typical cytokinin response.

61 ally relevant platform to controlled-release Ade and address large bone defects.

62 xoG:A can be repaired by enzymes that remove Ade opposite to template 8-oxoG, or 8-oxoG opposite to C

63 (2) The flipped target Ade binds to the surface of EcoDam in the absence of S-a

64 y DNA polymerases into DNA opposite template Ade.

65 ity that removes 8-oxoG opposite to template Ade.

66 reover, it is the first time to confirm that Ade mediates the osteogenesis of rat BMSCs through the S

67 The Ade-Thy pair binding at 40-45% loading reveals that Thy

68 (N)-A8 dihedral angle is 1.9 degrees and the Ade is virtually perpendicular to the corrin ring; in th

69 the corrin ring; in the minor conformer, the Ade is tilted down, and this dihedral is -48.7 degrees.

70 ptimal tracer candidate was selected for the Ade assay under buffer and realistic (diluted human seru

71 The partition ratio of the Ade formation (nonlethal event) to covalent acylation (l

72 Methylation of the Ade in GATC sequences regulates diverse bacterial cell f

73 In the absence of the Ade target, the binding of the labeled aptamers to SSB g

74 tion of the folded tertiary structure of the Ade-Apt-A complex triggered the release of the labeled n

75 ved one FU molecule and two molecules of the Ade-BTM functional monomer.

76 an arc from over C15 to over C12, while the Ade ring oscillates from perpendicular to parallel to th

77 -Ade) >/= 9-(tetrahydrofuryl)-adenine (9-THF-Ade; SQ 22,536), with the exception of Type II adenylyl

78 ce human cells do not readily convert Ado to Ade, an understanding of the substrate preferences of th

79 yses revealed direct binding of enoxolone to Ade.

80 1,2-dibromoethane were predominantly Gua to Ade transitions but, in the spectrum of such rifampicin-

81 nimizing incorporation of 8-oxoG opposite to Ade by DNA polymerases following adduct formation.

82 his coaxial drug-delivery system loaded with Ade provided a promising and clinically relevant platfor

83 pores of the MOF and become base-paired with Ade.

84 me x anti-Adenosine with Asp40-COO- [E(40) x Ade(a)], Enzyme x syn-Adenosine with Asp40-COOH [E(40H)

85 yme x syn-Adenosine with Asp40-COO- [E(40) x Ade(s)], and Enzyme x anti-Inosine with Asp40-COO- [E(40

86 tems with protonated Asp40, namely, E(40H) x Ade(a) and E(40H) x Ade(s), have zero SASA.

87 e x anti-Adenosine with Asp40-COOH [E(40H) x Ade(a)], Enzyme x anti-Adenosine with Asp40-COO- [E(40)

88 generated from the MD simulation of E(40H) x Ade(s) preserve the catalytically important hydrogen bon

89 Asp40, namely, E(40H) x Ade(a) and E(40H) x Ade(s), have zero SASA.

90 me x syn-Adenosine with Asp40-COOH [E(40H) x Ade(s)], Enzyme x syn-Adenosine with Asp40-COO- [E(40) x