ライフサイエンスコーパス: distamycin

1 non-covalently to the same AT-rich sites as distamycin.

2 P analog, when compared with the parent drug distamycin.

3 ased on the N-methyl pyrrole carboxamides of distamycin.

4 MGA1 proteins) by both monomeric and dimeric distamycin.

5 s of the sequence-specific binding molecule, distamycin.

6 which can be distinguished by sensitivity to distamycin.

7 beyond the initial studies on netropsin and distamycin.

8 hods and using the minor groove-binding drug distamycin.

9 -specific alkylating antitumor derivative of distamycin.

10 ubsequent incorporation into conjugates with distamycin A (1) are described.

11 cognate DNA than either the parent analogue, distamycin A (10-fold), or the structural isomer, f-PyIm

12 Distamycin A (Dist A) belongs to a class of drugs termed

13 rmed that f-ImPyIm is a stronger binder than distamycin A and f-PyImIm and that f-ImPyIm preferential

14 Both distamycin A and Hoechst 33258 can inhibit, to a similar

15 fferently by two minor groove-binding drugs, distamycin A and Hoechst 33258.

16 nor groove-binding drugs such as netropesin, distamycin A and Hoechst33258 and may be a reflection of

17 ove-binders, chromomycin A(3) (GC-specific), distamycin A and netropsin (both AT-specific), have been

18 he structurally related minor groove binders distamycin A and netropsin (K(i) </=1 microM).

19 T(pS)TT GCG) (A3T2) upon binding of the drug distamycin A at different stoichiometries.

20 Minor groove binding compounds related to distamycin A bind DNA with high sequence selectivity, re

21 y, it is shifted by 1 bp with respect to the distamycin A binding site on this DNA sequence.

22 we found that the GST-Cdc6 can compete with distamycin A for binding to the DNA molecule.

23 Distamycin A has been described as an inhibitor of the c

24 has a 10-fold greater affinity for CGCG than distamycin A has for its cognate, AATT.

25 quence appears to be weaker than that of the distamycin A homodimer to A/T sequences, most likely due

26 ith guanine tetrads of quadruplex DNA, while distamycin A interacts by binding to quadruplex grooves.

27 As distamycin A is a specific reagent that binds noncovalen

28 Distamycin A is a well known polyamide antibiotic that c

29 AT-binding Distamycin A largely blocks nuclear pore assembly, where

30 erminations of the binding mode of Tel01 and distamycin A to quadruplex oligonucleotides indicate tha

31 aled that binding of f-ImPyIm, f-PyImIm, and distamycin A to their respective hairpin cognate sequenc

32 ST-NP6 protein competes for DNA binding with distamycin A, an antibiotic that chelates DNA within the

33 stoichiometry, and mode of binding of Tel01, distamycin A, and diethylthiocarbocyanine iodide (DTC) t

34 Tel01, distamycin A, and DTC all form complexes with quadruplex

35 groove-binding drug chromomycin A3, but not distamycin A, disrupted Tax-enhanced CREB binding to the

36 An AT minor groove-binding drug, distamycin A, disrupted the TBP.TFIIA.DNA complex and re

37 This binding mode is similar to that of distamycin A, even though the dye lacks the hydrogen-bon

38 ing selectivity for several agents including distamycin A, netropsin, DAPI, Hoechst 33258, and bereni

39 ies of these agents were compared to that of distamycin A, using a fluorescence intercalator displace

40 the minor groove DNA-binding natural product distamycin A.

41 Distamycin, a minor groove binding drug, is very effecti

42 In contrast, a distamycin analogue with similar structure and charge an

43 In this report we describe a distamycin analogue, 2,2'-[4, 4'-[[aminocarbonyl]amino]b

44 ed complex of 2,3- bis(hydroxymethyl)pyrrole-distamycin and [d(CGCGAATTCGCG)]2.

45 AT-selective minor-groove binders, including distamycin and bisdistamycins, bisnetropsins, novel lexi

46 In addition, DAPI was more effective than distamycin and Hoechst 33258 at inhibiting the assembly

47 Distamycin and Hoechst 33258 have long served as the mod

48 ase I footprinting to examine the ability of distamycin and Hoechst 33258 to discriminate between dif

49 d only the AT bp in the binding sites, while distamycin and Hoechst protected these bp as well as fla

50 he basis for inhibition of vaccinia virus by distamycin and indicate that DNA minor-groove ligands ho

51 hree orders of magnitude more effective than distamycin and inhibited complexes between E2F1 and the

52 oove-binding ligands berenil, netropsin, and distamycin and the intercalating ligand acridine orange

53 HIV RT by minor groove binding drugs such as distamycin and their bis-linked derivatives.

54 Although netropsin, distamycin, and all other monomeric DNA binders showed w

55 nteraction of DNA binding drugs mithramycin, distamycin, and berenil with an intermolecular triplex f

56 NA-binding agents, such as ethidium bromide, distamycin, and doxorubicin, inhibit the formation of sl

57 equence specific ligands, such as netropsin, distamycin, and GLX, prefer uniform, narrow minor groove

58 nucleosome assembly only in the presence of distamycin, and increasing the number of 33-bp repeats i

59 Standard groove binding agents (DAPI, distamycin, and netropsin) showed a strong preference fo

60 -DNA binding, using the minor groove-binding distamycin as a model compound.

61 These results demonstrate the utility of distamycin as a probe of G4 DNA-protein interactions and

62 tude more effective than the natural product distamycin at inhibiting formation of complexes between

63 factor-DNA complex, was more effective than distamycin at preventing transcript formation.

64 However, the displaced AT hook alters distamycin binding by weakening the distamycin:DNA compl

65 The association phase of the distamycin binding reaction has not been studied in eith

66 Five prominent distamycin binding sites are noted within the c-Ki-ras p

67 Using NMR, we show that distamycin binds specifically to G4 DNA, stacking on the

68 Distamycin binds the minor groove of duplex DNA at AT-ri

69 At (A/T)10sites distamycin binds with similar affinity to T5A5, (TA)5and

70 HMGA1a was effectively displaced by distamycin, but the cooperative binding exhibited by dis

71 related to the linked bis-netropsins and bis-distamycins, but here, only one amino-pyrrole-carboxamid

72 We find that distamycin can also inhibit protein interactions with G-

73 rug concentrations of either mitoxantrone or distamycin completely blocked transcription, while low d

74 ared to the previous 2:1 all-IC d(ICICICIC)2-distamycin complex, the substitutions of the I x C base-

75 cognition elements not based on analogues of distamycin could be realized.

76 and poly(dIdC)2 and competitive binding with distamycin demonstrate that complex II is bound in the m

77 The minor groove binder distamycin did not displace 1 from HT DNA, suggesting th

78 tamycin:DNA complex, while slowing monomeric distamycin dissociation when AT hook is in excess.

79 k alters distamycin binding by weakening the distamycin:DNA complex, while slowing monomeric distamyc

80 DNA binding modes of distamycin (DST) were investigated via comparative bindi

81 The distamycin effect on transcription was mediated through

82 ye lacks the hydrogen-bonding groups used by distamycin for sequence-specific recognition.

83 groove binders (netropsin, Hoechst 33258 and distamycin) has shown the suitability of FSCE as a metho

84 s-linked lexitropsins based on netropsin and distamycin have been screened for their effectiveness in

85 two consensus sequences, either the expected distamycin hexamer binding sites followed by a CG base p

86 er for the I1L gene was partially reduced by distamycin; however, transcription from the intermediate

87 ber of 33-bp repeats increases the effect of distamycin in the destabilization of the nucleosome form

88 AT-rich repeating DNAs derived from the rare distamycin-inducible site, FRA16B, was examined for its

89 The minor groove binders netropsin and distamycin inhibited oxopropenylation, but methyl green,

90 Antibody ablation, distamycin inhibition of binding, renaturation and compe

91 In contrast, AT-binding drugs (e.g., distamycin) interfered only with E2F1-DNA complex format

92 We show here that distamycin is a potent inhibitor of vaccinia virus repli

93 Distamycin is an antibiotic that also binds A/T-rich DNA

94 Distamycin is an antibiotic that specifically targets th

95 tructures of the side-by-side binding of two distamycin molecules to the DNA octamers d(ICITACIC)2 an

96 minor groove binding ligands (Hoechst 33258, distamycin, netropsin and berenil) with DNA fragments wh

97 Minor groove binding ligands, such as distamycin, netropsin, and GLX, an indole-linked dimer o

98 ial for the side-by-side binding mode of the distamycin/netropsin family of drugs.

99 Neither distamycin nor berenil prevents triplex formation, and,

100 n expression, we have examined the effect of distamycin on the cytokine-induced E-selectin expression

101 We characterized the effect of distamycin on vaccinia virus nucleic acid biosynthesis w

102 on, and, furthermore, the addition of either distamycin or berenil to the pre-formed triplex structur

103 We found that distamycin prolonged E-selectin expression, both by sust

104 to single-strand oligonucleotide ions, while distamycin/quadruplex complexes fragment into single-str

105 d by Me-lex are 3-MeA; 2) the co-addition of distamycin quantitatively inhibited methylation at all m

106 Distamycin shows extremely fast association with the 1:1

107 We find that in (A/T)6tracts distamycin shows little discrimination between the vario

108 GA1a is displaced from the DNA by 1 equiv of distamycin, suggesting the ability to develop therapeuti

109 quadruplex complexes are similar to those of distamycin; therefore, it is concluded that DTC interact

110 accompanied by a small red shift, on binding distamycin to its specific target sites.

111 likely to be due to preferential binding of distamycin to the minor groove of the DNA duplex as oppo

112 Polyamides (PAs) are distamycin-type ligands of DNA that bind the minor groov

113 nscription was observed when mitoxantrone or distamycin was added either before or after assembly of

114 ustard and imidazole-containing analogues of distamycin was determined using modified sequencing tech

115 in, but the cooperative binding exhibited by distamycin was eliminated by displaced HMGA1a.

116 Inhibition of binding by the antibiotic distamycin, which binds in the minor groove of A/T-rich

117 Distamycin, which, like the AT-hook DNA binding motif fo