Chromatin Remodeling and Nuclear Receptor Signaling

被引:8
作者
Buranapramest, Manop [1 ]
Chakravarti, Debabrata [1 ]
机构
[1] Northwestern Univ, Robert H Lurie Comprehens Canc Ctr, Feinberg Sch Med, Div Reprod Biol Res,Dept Obstet & Gynecol, Chicago, IL 60611 USA
来源
REGULATORY MECHANISMS IN TRANSCRIPTIONAL SIGNALING | 2009年 / 87卷
关键词
THYROID-HORMONE RECEPTOR; HISTONE ACETYLTRANSFERASE ACTIVITY; REV-ERB-ALPHA; ACUTE UNDIFFERENTIATED LEUKEMIA; HUMAN GLUCOCORTICOID RECEPTOR; ADENOVIRAL ONCOPROTEIN E1A; HUMAN ESTROGEN-RECEPTOR; RETINOIC ACID RECEPTOR; N-COR COMPLEX; TRANSCRIPTIONAL REPRESSION;
D O I
10.1016/S1877-1173(09)87006-3
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
070307 [化学生物学]; 071010 [生物化学与分子生物学];
摘要
Nuclear receptors (NRs) constitute a large family of ligand-dependent transcription factors that play key roles in development, differentiation, metabolism, and homeostasis. They participate in these processes by coordinating and regulating the expression of their target genes. The eukaryotic genome is packaged as chromatin and is generally inhibitory to the process of transcription. NRs overcome this barrier by recruiting two classes of chromatin remodelers, histone modifying enzymes and ATP-dependent chromatin remodelers. These remodelers alter chromatin structure at target gene promoters by post-translational modification of histone tails and by disrupting DNA-histone interactions, respectively. In the presence of ligand, NRs promote transcription by recruiting remodeling enzymes that increase promoter accessibility to the basal transcription machinery. In the absence of ligand a subset of NRs recruit remodelers that establish and maintain a closed chromatin environment, to ensure efficient gene silencing. This chapter reviews the chromatin remodeling enzymes associated with NR gene control, with an emphasis on the mechanisms of NR-mediated repression.
引用
收藏
页码:193 / 234
页数:42
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