| First Author | Li FQ | Year | 2007 |
| Journal | Mol Cell Biol | Volume | 27 |
| Issue | 12 | Pages | 4347-54 |
| PubMed ID | 17403895 | Mgi Jnum | J:122334 |
| Mgi Id | MGI:3714087 | Doi | 10.1128/MCB.01640-06 |
| Citation | Li FQ, et al. (2007) Chibby promotes adipocyte differentiation through inhibition of beta-catenin signaling. Mol Cell Biol 27(12):4347-54 |
| abstractText | The canonical Wnt/beta-catenin signaling pathway plays diverse roles in embryonic development and disease. Activation of this pathway, likely by Wnt-10b, has been shown to inhibit adipogenesis in cultured 3T3-L1 preadipocytes and in mice. Here, we report that the beta-catenin antagonist Chibby (Cby) is required for adipocyte differentiation. Cby is expressed in adipose tissue in mice, and Cby protein levels increase during adipogenic differentiation of 3T3-L1 cells. Ectopic expression of Cby induces spontaneous differentiation of these cells into mature adipocytes to an extent similar to that of dominant-negative Tcf-4. In contrast, depletion of Cby by RNA interference potently blocks adipogenesis of 3T3-L1 and mouse embryonic stem cells. In support of this, embryonic fibroblasts obtained from Cby-deficient embryos display attenuated differentiation to the adipogenic lineage. Mechanistically, Cby promotes adipocyte differentiation, in part by inhibiting beta-catenin, since gain or loss of function of Cby influences beta-catenin signaling in 3T3-L1 cells. Our results therefore establish Cby as a novel proadipogenic factor required for adipocyte differentiation. |
