NRs (nuclear receptors) regulate the expression of specific gene networks in target cells by recruiting cofactor complexes involved in chromatin remodelling and in the assembly of transcription complexes. The importance of activating gene expression, in metabolic tissues, is well established, but the contribution of transcriptional inhibition is less well defined. In this review, we highlight a crucial role for RIP140 (receptor-interacting protein 140), a transcriptional co-repressor for NR, in the regulation of metabolic gene expression. Many genes involved in lipid and carbohydrate metabolism are repressed by RIP140 in adipose and muscle. The repressive function of RIP140 results from its ability to bridge NRs to repressive enzyme complexes that modify DNA and histones. In the absence of RIP140, expression from many metabolic genes is increased so that mice exhibit a lean phenotype and resistance to high-fat-diet-induced obesity and display increased glucose tolerance and insulin sensitivity. We propose that a functional interplay between transcriptional activators and the co-repressor RIP140 is an essential process in metabolic regulation.
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December 2006
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Conference Article|
October 25 2006
The nuclear receptor co-repressor RIP140 controls the expression of metabolic gene networks
M.G. Parker;
M.G. Parker
1
1To whom correspondence should be addressed (email m.parker@imperial.ac.uk).
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M. Christian;
M. Christian
1Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, U.K.
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R. White
R. White
1Institute of Reproductive and Developmental Biology, Faculty of Medicine, Imperial College London, Du Cane Road, London W12 0NN, U.K.
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Publisher: Portland Press Ltd
Received:
August 07 2006
Online ISSN: 1470-8752
Print ISSN: 0300-5127
© 2006 The Biochemical Society
2006
Biochem Soc Trans (2006) 34 (6): 1103–1106.
Article history
Received:
August 07 2006
Citation
M.G. Parker, M. Christian, R. White; The nuclear receptor co-repressor RIP140 controls the expression of metabolic gene networks. Biochem Soc Trans 1 December 2006; 34 (6): 1103–1106. doi: https://doi.org/10.1042/BST0341103
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