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类固醇激素受体介导的小鼠乳腺肿瘤病毒启动子处的组蛋白去乙酰化与转录

Steroid hormone receptor-mediated histone deacetylation and transcription at the mouse mammary tumor virus promoter.

作者信息

Sheldon L A, Becker M, Smith C L

机构信息

Department of Physiology, Dartmouth Medical School, Lebanon, New Hampshire 03756, USA.

出版信息

J Biol Chem. 2001 Aug 31;276(35):32423-6. doi: 10.1074/jbc.C100315200. Epub 2001 Jul 11.

Abstract

Acetylation of lysines in histones H3 and H4 N-terminal tails is associated with transcriptional activation and deacetylation with repression. Our studies with the mouse mammary tumor virus (MMTV) promoter in chromatin show significant levels of acetylation at promoter proximal and distal regions prior to transactivation. Upon activation with glucocorticoids or progestins, promoter proximal histones become deacetylated within the region of inducible nuclease hypersensitivity. The deacetylation lags behind the initiation of transcription, indicating a role in post-activation regulation. Our results indicate a novel mechanism by which target promoters are regulated by steroid receptors and chromatin modification machinery.

摘要

组蛋白H3和H4 N端尾部赖氨酸的乙酰化与转录激活相关,而去乙酰化则与转录抑制相关。我们对染色质中鼠乳腺肿瘤病毒(MMTV)启动子的研究表明,在反式激活之前,启动子近端和远端区域存在显著水平的乙酰化。在用糖皮质激素或孕激素激活后,启动子近端组蛋白在可诱导核酸酶超敏反应区域内发生去乙酰化。去乙酰化滞后于转录起始,表明其在激活后调节中发挥作用。我们的结果表明了一种新的机制,通过该机制靶启动子受类固醇受体和染色质修饰机制的调控。

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