RIP140-targeted repression of gene expression in adipocytes

Mark Christian, Evangelos Kiskinis, Darja Debevec, Göran Leonardsson, Roger White, Malcolm G. Parker*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

150 Scopus citations


Ligand-dependent repression of nuclear receptor activity forms a novel mechanism for regelating gene expression. To investigate the intrinsic role of the corepressor RIP140, we have monitored gene expression profiles in cells that express or lack the RIP140 gene and that can be induced to undergo adipogenesis in vitro. In contrast to normal white adipose tissue and in vitro-differentiated wild-type adipocytes, RIP140-null cells show elevated energy expenditure and express high levels of the uncoupling protein 1 gene (Ucp1), carnitine palmitoyltransferase 1b, and the cell-death-inducing DFF45-like effector A. Conversely, all these changes are abrogated by the reexpression of RIP140. Analysis of the Ucp1 promoter showed RIP140 recruitment to a key enhancer element, demonstrating a direct role in repressing gene expression. Therefore, reduction in the levels of RIP140 or prevention of its recruitment to nuclear receptors may provide novel mechanisms for the control of energy expenditure in adipose cells.

Original languageEnglish (US)
Pages (from-to)9383-9391
Number of pages9
JournalMolecular and cellular biology
Issue number21
StatePublished - Nov 2005

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology


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