4.6 Article

Loss of the Prader-Willi obesity syndrome protein necdin promotes adipogenesis

Journal

GENE
Volume 497, Issue 1, Pages 45-51

Publisher

ELSEVIER
DOI: 10.1016/j.gene.2012.01.027

Keywords

Genetic obesity; Mouse embryonic fibroblast; Adipogenesis

Funding

  1. Canadian Institutes of Health Research [MOP160321]
  2. Alberta Innovates: Health Solutions

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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. (C) 2012 Elsevier B.V. All rights reserved.

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