嵌入药物对聚（dG-dC）从B型到Z型转变动力学的影响。
The effect of intercalating drugs on the kinetics of the B to Z transition of poly(dG-dC).
作者信息
Mirau P A, Kearns D R
出版信息
Nucleic Acids Res. 1983 Mar 25;11(6):1931-41. doi: 10.1093/nar/11.6.1931.
Abstract
We have measured the ability of the intercalating drugs proflavine, ethidium bromide, actinomycin D, and bismethidiumspermine to inhibit the salt induced transition of poly(dG-dC) from the B to the Z form. While all of the drugs studied slowed the B to Z transition, the effectiveness of the drugs correlates much better with their DNA binding kinetics than their DNA binding constants. In studies where the binding densities of ethidium and actinomycin were varied we have found that high levels of ethidium, more than 1 per 20 base pairs, were required to inhibit the B to Z transition while low levels of actinomycin, less than 1 per 450 base pairs, reduced the transition rate. Studies of the B to Z transition in the presence of both actinomycin and ethidium suggest that the drugs inhibit the transition by different mechanisms. The results are interpreted in terms of a modification of the kinetic model proposed by Pohl and Jovin in which, depending on the DNA binding kinetics of the drug, the drug may inhibit nucleation and/or propagation of the B to Z transition.
摘要
我们已测定了嵌入药物原黄素、溴化乙锭、放线菌素D和双甲脒精胺抑制盐诱导的聚（dG-dC）从B型向Z型转变的能力。虽然所研究的所有药物都减缓了B型向Z型的转变，但药物的有效性与其DNA结合动力学的相关性远高于其DNA结合常数。在改变溴化乙锭和放线菌素结合密度的研究中，我们发现，抑制B型向Z型转变需要高水平的溴化乙锭（每20个碱基对超过1个），而低水平的放线菌素（每450个碱基对少于1个）就能降低转变速率。在同时存在放线菌素和溴化乙锭的情况下对B型向Z型转变的研究表明，这两种药物通过不同机制抑制转变。根据Pohl和Jovin提出的动力学模型的修正来解释这些结果，其中，根据药物的DNA结合动力学，药物可能抑制B型向Z型转变的成核和/或传播。
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