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First published online 14 February 2006
doi: 10.1242/jcs.02792

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PKB is required for adipose differentiation of mouse embryonic fibroblasts

Friedrich Miescher Institute for Biomedical Research, Maulbeerstr. 66, CH-4058, Basel, Switzerland

^* Author for correspondence (e-mail: hemmings{at}fmi.ch)

Accepted 14 November 2005

Protein kinase B (PKB) is a key regulator of metabolism, proliferation and differentiation. We have explored the role of PKB in adipogenesis using wild-type and PKB-knockout mouse embryonic fibroblasts (MEFs) and show that lack of PKB prevents MEF differentiation into adipocytes. Expression of ectopic PKB in PKB-deficient cells restores adipogenesis. We identified 80 genes whose expression was upregulated in wild-type MEFs during adipogenesis but whose expression was significantly reduced in PKB-deficient MEFs under the same conditions. Significantly, the regulator of adipogenesis Krüppel-like transcription factor 15 gene expression was downregulated in PKB-deficient MEFs but could be restored by expressing an active PKB in the deficient cells. The level of lipocalin 2, renin 1 and receptor-activity-modifying protein 3 genes expressed by adipose cells was also decreased in PKB-deficient MEFs, and are inhibited by LY294002 treatment during early adipocyte differentiation of 3T3-L1 cells. The results underscore an essential role for PKB in the transcriptional program required for adipogenesis.

Key words: PKB, Adipocyte differentiation, Mouse embryonic fibroblasts, Microarray analysis

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