共 80 条
Nuclear receptor transrepression pathways that regulate inflammation in macrophages and T cells
被引:483
作者:

Glass, Christopher K.
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
Univ Calif San Diego, Dept Med, Sch Med, La Jolla, CA 92093 USA Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA

Saijo, Kaoru
论文数: 0 引用数: 0
h-index: 0
机构:
Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
机构:
[1] Univ Calif San Diego, Dept Cellular & Mol Med, La Jolla, CA 92093 USA
[2] Univ Calif San Diego, Dept Med, Sch Med, La Jolla, CA 92093 USA
关键词:
NF-KAPPA-B;
GLUCOCORTICOID-RECEPTOR;
GENE-EXPRESSION;
INSULIN-RESISTANCE;
ADIPOSE-TISSUE;
PPAR-GAMMA;
MEDIATES TRANSREPRESSION;
CO-REPRESSOR;
LXR-BETA;
COREPRESSOR;
D O I:
10.1038/nri2748
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Members of the nuclear receptor superfamily of ligand-dependent transcription factors regulate diverse aspects of immunity and inflammation by both positively and negatively regulating gene expression. Here, we review recent studies providing insights into the distinct mechanisms that enable nuclear receptors to antagonize pro-inflammatory programmes of gene expression in macrophages and T cells by altering the turnover or recruitment of co-repressors and co-activators in a gene-specific manner. These nuclear receptor-dependent transrepression pathways are proposed to have roles in controlling the initiation, magnitude and duration of pro-inflammatory gene expression and are amenable to pharmacological manipulation.
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页码:365 / 376
页数:12
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