Suppr超能文献

一种β细胞特异性蛋白与胰岛素基因增强子的两个主要调控序列结合。

A beta-cell-specific protein binds to the two major regulatory sequences of the insulin gene enhancer.

作者信息

Ohlsson H, Karlsson O, Edlund T

机构信息

Department of Microbiology, University of Umeå, Sweden.

出版信息

Proc Natl Acad Sci U S A. 1988 Jun;85(12):4228-31. doi: 10.1073/pnas.85.12.4228.

Abstract

The selective transcription of the Rat insulin 1 gene is mainly dependent on a beta-cell-specific enhancer element located in the 5' flanking DNA. In analogy to many other viral and cellular enhancers, the insulin enhancer has been shown to be of a mosaic structure and the cis-acting elements of importance for the enhancer activity have been defined. Two short sequences are of crucial importance for the enhancer activity since mutation of either sequence leads to a decrease in activity (by a factor of approximately 10), and the double mutant eliminates all enhancer activity. This study shows that these two major cis-acting elements interact with beta-cell-specific proteins. These two enhancer modules carry an 8-base-pair homology and compete with each other for protein binding, suggesting that they interact with the same protein, designated insulin enhancer binding factor 1 (IEF 1). Since mutation of these sequences eliminates the enhancer activity and protein binding, we propose that IEF 1 is the key regulator controlling the selective activity of the insulin gene enhancer.

摘要

大鼠胰岛素1基因的选择性转录主要依赖于位于5'侧翼DNA中的β细胞特异性增强子元件。与许多其他病毒和细胞增强子类似,胰岛素增强子已被证明具有镶嵌结构,并且已确定了对增强子活性重要的顺式作用元件。两个短序列对增强子活性至关重要,因为任一序列的突变都会导致活性降低(约为10倍),而双突变则消除了所有增强子活性。本研究表明,这两个主要的顺式作用元件与β细胞特异性蛋白相互作用。这两个增强子模块具有8个碱基对的同源性,并相互竞争蛋白质结合,表明它们与同一种蛋白质相互作用,该蛋白质被命名为胰岛素增强子结合因子1(IEF 1)。由于这些序列的突变消除了增强子活性和蛋白质结合,我们提出IEF 1是控制胰岛素基因增强子选择性活性的关键调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba2f/280400/d9fe5b8ec518/pnas00264-0123-a.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验