| First Author | Baudry A | Year | 2006 |
| Journal | J Cell Sci | Volume | 119 |
| Issue | Pt 5 | Pages | 889-97 |
| PubMed ID | 16478789 | Mgi Jnum | J:106565 |
| Mgi Id | MGI:3618974 | Doi | 10.1242/jcs.02792 |
| Citation | Baudry A, et al. (2006) PKBalpha is required for adipose differentiation of mouse embryonic fibroblasts. J Cell Sci 119(Pt 5):889-97 |
| abstractText | Protein kinase Balpha (PKBalpha) is a key regulator of metabolism, proliferation and differentiation. We have explored the role of PKBalpha in adipogenesis using wild-type and PKBalpha-knockout mouse embryonic fibroblasts (MEFs) and show that lack of PKBalpha prevents MEF differentiation into adipocytes. Expression of ectopic PKBalpha in PKBalpha-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 PKBalpha-deficient MEFs under the same conditions. Significantly, the regulator of adipogenesis Kruppel-like transcription factor 15 gene expression was downregulated in PKBalpha-deficient MEFs but could be restored by expressing an active PKBalpha 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 PKBalpha-deficient MEFs, and are inhibited by LY294002 treatment during early adipocyte differentiation of 3T3-L1 cells. The results underscore an essential role for PKBalpha in the transcriptional program required for adipogenesis. |
