| First Author | Bush JR | Year | 2012 |
| Journal | Gene | Volume | 497 |
| Issue | 1 | Pages | 45-51 |
| PubMed ID | 22305984 | Mgi Jnum | J:183684 |
| Mgi Id | MGI:5319101 | Doi | 10.1016/j.gene.2012.01.027 |
| Citation | Bush JR, et al. (2012) Loss of the Prader-Willi obesity syndrome protein necdin promotes adipogenesis. Gene 497(1):45-51 |
| abstractText | We investigated the role of necdin during adipogenic differentiation. Necdin is one of several genes inactivated in children with Prader-Willi syndrome, who are predisposed to increased adiposity at the expense of lean mass. Necdin promotes neuronal and muscle differentiation and survival through interactions with a variety of proteins, including cell surface receptors, modifiers of protein stability, and transcription factors. In pre-adipocytes, necdin over-expression inhibits adipogenesis, while reducing necdin levels enhances adipogenic differentiation in tissue culture cells. We now directly demonstrate a role for necdin in inhibiting adipogenesis using cells derived from necdin deficient mice. |
