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Journal of Lipid Research, Vol. 49, 2535-2544, December 2008
Copyright © 2008 by American Society for Biochemistry and Molecular Biology

HRASLS3 is a PPAR-selective target gene that promotes adipocyte differentiation^*

Sarah Hummasti, Cynthia Hong, Steven J. Bensinger and Peter Tontonoz¹

Howard Hughes Medical Institute, Department of Pathology and Laboratory Medicine, University of California, Los Angeles, CA

^* The authors have no financial interest related to this work.

Published, JLR Papers in Press, July 29, 2008.

¹ To whom correspondence should be addressed. e-mail: ptontonoz{at}mednet.ucla.edu

The prevalence of obesity and its associated metabolic diseases worldwide has focused attention on understanding the mechanisms underlying adipogenesis. The nuclear receptor PPAR has emerged as a central regulator of adipose tissue function and formation. Despite the identification of numerous PPAR targets involved in a range of processes, from lipid droplet formation to adipokine secretion, information is still lacking on targets downstream of PPAR that directly affect fat cell differentiation. Here we identify HRASLS3 as a novel PPAR regulated gene with a role in adipogenesis. HRASLS3 expression increases during the differentiation of preadipocyte cell lines and is highly expressed in white and brown adipose tissue in mice. HRASLS3 expression is induced by PPAR ligands in preadipocyte cell lines as well in adipose tissue in vivo. We demonstrate that the HRASLS3 promoter contains a functional PPAR response element and is a direct target for regulation by PPAR/RXR heterodimers. Finally, we show that overexpression of HRASLS3 augments PPAR-driven lipid accumulation and adipogenesis, whereas siRNA-mediated knockdown of HRASLS3 expression decreases differentiation. Together, these results identify HRASLS3 as one of the downstream effectors of PPAR action in adipogenesis.

Supplementary key words nuclear receptor • adipogenesis • lipid metabolism

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