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.
Department of Medical Genetics, University of Alberta, Edmonton, AB, Canada.
Jason Russell
JR
Bush
Rachel
R
Wevrick
D048868:Adaptor Proteins, Signal Transducing; D050156:Adipogenesis; D000818:Animals; D002460:Cell Line; D018925:Chemokines; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins / Q000378:metabolism; D051379:Mice; D018345:Mice, Knockout; D009419:Nerve Tissue Proteins / Q000235:genetics / Q000502:physiology*; D009687:Nuclear Proteins / Q000235:genetics / Q000502:physiology*; D009765:Obesity / Q000235:genetics*; D011218:Prader-Willi Syndrome / Q000235:genetics*
D048868:Adaptor Proteins, Signal Transducing; D018925:Chemokines; C498624:DKK3 protein, human; D036341:Intercellular Signaling Peptides and Proteins; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; C069766:necdin