Binding of distamycin A to UV-damaged DNA

被引：5

作者：

Inase, A

Kodama, TS

Sharif, J

Xu, Y

Ayame, H

Sugiyama, H

Iwai, S

机构：

[1] Osaka Univ, Grad Sch Engn Sci, Div Chem, Toyonaka, Osaka 5608531, Japan

[2] JBIRC, JBIC, Koto Ku, Tokyo 1350064, Japan

[3] Biomol Engn Res Inst, Suita, Osaka 5650874, Japan

[4] Univ Tokyo, Sch Engn, Dept Chem & Biotechnol, Bunkyo Ku, Tokyo 1138656, Japan

[5] Tokyo Med & Dent Univ, Inst Biomat & Bioengn, Div Biofunct Mol, Chiyoda Ku, Tokyo 1010062, Japan

[6] Kyoto Univ, Grad Sch Sci, Dept Chem, Sakyo Ku, Kyoto 6068502, Japan

来源：

JOURNAL OF THE AMERICAN CHEMICAL SOCIETY | 2004年 / 126卷 / 35期

关键词：

D O I：

10.1021/ja048851k

中图分类号：

O6 [化学];

学科分类号：

0703 ;

摘要：

We have found that distamycin A can bind to DNA duplexes containing the (6-4) photoproduct, one of the major UV lesions in DNA, despite the changes, caused by photoproduct formation, in both the chemical structure of the base moiety and the local tertiary structure of the helix. A 20-mer duplex containing the target site, AATT(.)AATT, was designed, and then one of the TT sequences was changed to the (6-4) photoproduct. Distamycin binding to the photoproduct-containing duplex was detected by CD spectroscopy, whereas specific binding did not occur when the TT site was changed to a cyclobutane pyrimidine dimer, another type of UV lesion. Distamycin binding was analyzed in detail using 14-mer duplexes. Curve fitting of the CD titration data and induced CD difference spectra revealed that the binding stoichiometry changed from 1:1 to 2:1 with photoproduct formation. Melting curves of the drug-DNA complexes also supported this stoichiometry.

引用

页码：11017 / 11023

页数：7

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