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Mot1是RNA聚合酶II转录的全局阻遏物,通过一种ATP依赖机制抑制TBP与DNA的结合。

Mot1, a global repressor of RNA polymerase II transcription, inhibits TBP binding to DNA by an ATP-dependent mechanism.

作者信息

Auble D T, Hansen K E, Mueller C G, Lane W S, Thorner J, Hahn S

机构信息

Fred Hutchinson Cancer Research Center, Seattle, Washington 98104.

出版信息

Genes Dev. 1994 Aug 15;8(16):1920-34. doi: 10.1101/gad.8.16.1920.

Abstract

Basal transcription of many genes in yeast is repressed by Mot1, an essential protein which is a member of the Snf2/Swi2 family of conserved nuclear factors. ADI is an ATP-dependent inhibitor of TATA-binding protein (TBP) binding to DNA that inhibits transcription in vitro. Here we demonstrate that ADI is encoded by the MOT1 gene. Mutation of MOT1 abolishes ADI activity and derepresses basal transcription in vitro and in vivo. Recombinant Mot1 removes TBP from DNA and Mot1 contains an ATPase activity which is essential for its function. Genetic interactions between Mot1 and TBP indicate that their functions are interlinked in vivo. These results provide a general model for understanding the mechanism of action of a large family of nuclear factors involved in processes such as transcription and DNA repair.

摘要

酵母中许多基因的基础转录受Mot1抑制,Mot1是一种必需蛋白,属于保守核因子的Snf2/Swi2家族。ADI是一种依赖ATP的TATA结合蛋白(TBP)与DNA结合的抑制剂,可在体外抑制转录。在此我们证明ADI由MOT1基因编码。MOT1的突变消除了ADI活性,并在体外和体内解除了基础转录的抑制。重组Mot1可从DNA上移除TBP,且Mot1含有一种对其功能至关重要的ATP酶活性。Mot1和TBP之间的遗传相互作用表明它们在体内的功能相互关联。这些结果为理解参与转录和DNA修复等过程的一大类核因子的作用机制提供了一个通用模型。

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