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腺病毒核心蛋白和染色质组装因子将超螺旋引入DNA

Introduction of superhelical turns into DNA by adenoviral core proteins and chromatin assembly factors.

作者信息

Burg J L, Schweitzer J, Daniell E

出版信息

J Virol. 1983 Jun;46(3):749-55. doi: 10.1128/JVI.46.3.749-755.1983.

Abstract

The interaction in vitro between adenoviral histone-like proteins and DNA in the presence of chromatin assembly factors was investigated. Viral core protein VII or its precursor pVII was incubated with DNA in the presence of an extract of HeLa cell chromatin, which mediates nucleosome assembly from histones and DNA. We have demonstrated that either protein can introduce superhelical turns into relaxed closed-circular DNA and that the presence of chromatin extract is necessary for the supertwisting effect. A greater density of superhelical turns was produced by pVII than by VII, but neither protein-DNA interaction resulted in the "physiological" amount of supertwisting produced by histones. The inhibition of histone-induced supercoiling by both proteins and the protection of turns in supertwisted starting material are also described. The nucleosome assembly factor, nucleoplasmin, fails to mediate the introduction of superhelical turns by VII or pVII.

摘要

研究了在染色质组装因子存在的情况下腺病毒组蛋白样蛋白与DNA在体外的相互作用。病毒核心蛋白VII或其前体pVII在HeLa细胞染色质提取物存在的情况下与DNA一起孵育,该提取物介导由组蛋白和DNA组装核小体。我们已经证明,这两种蛋白都能将超螺旋引入松弛的闭环DNA中,并且染色质提取物的存在对于超螺旋效应是必需的。pVII产生的超螺旋密度比VII更高,但两种蛋白与DNA的相互作用都没有产生组蛋白所产生的“生理”超螺旋量。还描述了这两种蛋白对组蛋白诱导的超螺旋的抑制作用以及对超螺旋起始材料中螺旋的保护作用。核小体组装因子核质蛋白不能介导VII或pVII引入超螺旋。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2073/256551/6fde6d6debfe/jvirol00147-0081-a.jpg

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