Epigenetic Mechanisms of the Glucocorticoid Receptor

被引:58
作者
Bartlett, Andrew A. [1 ]
Lapp, Hannah E. [1 ]
Hunter, Richard G. [1 ]
机构
[1] Univ Massachusetts, Dept Psychol, 100 Morrissey Blvd, Boston, MA 02125 USA
关键词
HISTONE DEACETYLASE 1; DNA-METHYLATION; GENE ACTIVATION; ACUTE STRESS; MEMORY FORMATION; BINDING-SITES; DENTATE GYRUS; COACTIVATOR; EXPRESSION; TRANSCRIPTION;
D O I
10.1016/j.tem.2019.07.003
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The glucocorticoid receptor (GR) has been shown to be important for mediating cellular responses to stress and circulating glucocorticoids. Ligand-dependent transcriptional changes induced by GR are observed across numerous tissues. However, the mechanisms by which GR achieves cell and tissue-specific effects are less clear. Epigenetic mechanisms have been proposed to explain some of these differences as well as some of the lasting, even transgenerational, effects of stress and glucocorticoid action. GR functions in tandem with epigenetic cellular machinery to coordinate transcription and shape chromatin structure. Here, we describe GR interactions with these effectors and how GR acts to reshape the epigenetic landscape in response to the environment.
引用
收藏
页码:807 / 818
页数:12
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