The metabolic coregulator RIP140: an update

被引:61
作者
Fritah, Asmaa [1 ]
Christian, Mark [1 ]
Parker, Malcolm G. [1 ]
机构
[1] Univ London Imperial Coll Sci Technol & Med, Inst Reprod & Dev Biol, Fac Med, London W12 0NN, England
来源
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM | 2010年 / 299卷 / 03期
关键词
receptor-interacting protein-140; corepressor; coactivator; transcription; cytoplasm; nuclear receptors; metabolism; adipose tissue; skeletal muscle; mitochondria; RECEPTOR-INTERACTING PROTEIN-140; TRANSCRIPTIONAL COREPRESSOR RIP140; NUCLEAR RECEPTOR; OXIDATIVE-METABOLISM; ARGININE METHYLATION; CARDIAC-HYPERTROPHY; ESTROGEN-RECEPTOR; SKELETAL-MUSCLE; GENE-EXPRESSION; REPRESSOR;
D O I
10.1152/ajpendo.00243.2010
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Fritah A, Christian M, Parker MG. The metabolic coregulator RIP140: an update. Am J Physiol Endocrinol Metab 299: E335-E340, 2010. First published June 8, 2010; doi:10.1152/ajpendo.00243.2010.-RIP140 is a transcriptional coregulator highly expressed in metabolic tissues where it has important and diverse actions. RIP140-null mice show that it plays a crucial role in the control of lipid metabolism in adipose tissue, skeletal muscle, and the liver and is essential for female fertility. RIP140 has been shown to act as a ligand-dependent transcriptional corepressor for metabolic nuclear receptors such as estrogen-related receptors and peroxisome proliferator-activated receptors. The role of RIP140 as a corepressor has been strengthened by the characterization of RIP140-overexpressing mice, although it emerges through several studies that RIP140 can also behave as a coactivator. Nuclear localization of RIP140 is important for controlling transcription of target genes and is subject to regulation by posttranslational modifications. However, cytoplasmic RIP140 has been shown to play a role in the control of metabolism through direct regulation of glucose transport in adipocytes. In this review, we focus on recent advances highlighting the growing importance of RIP140 as a regulator of energy homeostasis.
引用
收藏
页码:E335 / E340
页数:6
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