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

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.
AuthorsJason Russell Bush, Rachel Wevrick
JournalGene (Gene) Vol. 497 Issue 1 Pg. 45-51 (Apr 10 2012) ISSN: 1879-0038 [Electronic] Netherlands
PMID22305984 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2012 Elsevier B.V. All rights reserved.
Chemical References
  • DKK3 protein, human
  • Intercellular Signaling Peptides and Proteins
  • Nerve Tissue Proteins
  • Nuclear Proteins
  • necdin
  • Adipogenesis
  • Animals
  • Cell Line
  • Humans
  • Intercellular Signaling Peptides and Proteins (metabolism)
  • Mice
  • Mice, Knockout
  • Nerve Tissue Proteins (genetics, physiology)
  • Nuclear Proteins (genetics, physiology)
  • Obesity (genetics)
  • Prader-Willi Syndrome (genetics)

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