Huang Y Q, Rehfuss R P, LaPlante S R, Boudreau E, Borer P N, Lane M J
Department of Medicine, State University of New York, Syracuse 13210.
Nucleic Acids Res. 1988 Dec 9;16(23):11125-39. doi: 10.1093/nar/16.23.11125.
Two DNA hexadecamers containing one central 5'-GC-3' base step have been examined by footprinting methodology in the presence and absence of actinomycin D. The results of these studies, coupled with imino proton NMR measurements indicate that the antitumor drug causes a change in DNA conformation at a distance from the actinomycin intercalation site in a molecule of sequence d[ATATATAGCTATATAT] that does not occur in d[AAAAAAAGCTTTTTTT]. The experiments demonstrate that DNase I rate enhancements associated with actinomycin D binding are caused by ligand alteration of equilibrium DNA structure.
采用足迹法对两个含有一个中心5'-GC-3'碱基步的DNA十六聚体进行了研究，实验中分别加入和不加入放线菌素D。这些研究结果与亚氨基质子核磁共振测量结果表明，在序列为d[ATATATAGCTATATAT]的分子中，这种抗肿瘤药物在距放线菌素嵌入位点一定距离处引起DNA构象变化，而在d[AAAAAAAGCTTTTTTT]中则不会发生这种变化。实验表明，与放线菌素D结合相关的DNase I速率增强是由配体对DNA平衡结构的改变引起的。
