Abstract |
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.
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Authors | Jason Russell Bush, Rachel Wevrick |
Journal | Gene
(Gene)
Vol. 497
Issue 1
Pg. 45-51
(Apr 10 2012)
ISSN: 1879-0038 [Electronic] Netherlands |
PMID | 22305984
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 2012 Elsevier B.V. All rights reserved. |
Chemical References |
- Adaptor Proteins, Signal Transducing
- Chemokines
- DKK3 protein, human
- Intercellular Signaling Peptides and Proteins
- Nerve Tissue Proteins
- Nuclear Proteins
- necdin
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Topics |
- Adaptor Proteins, Signal Transducing
- Adipogenesis
- Animals
- Cell Line
- Chemokines
- 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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