Loss-of-function mutations in SIM1 contribute to obesity and Prader-Willi–like features-Reference-Cited by-同舟云学术

Loss-of-function mutations in SIM1 contribute to obesity and Prader-Willi–like features

Published:2013-06-17 Issue:7 Volume:123 Page:3037-3041
ISSN:0021-9738
Container-title:Journal of Clinical Investigation
language:en
Short-container-title:J. Clin. Invest.

Author:

Bonnefond Amélie,Raimondo Anne,Stutzmann Fanny,Ghoussaini Maya,Ramachandrappa Shwetha,Bersten David C.,Durand Emmanuelle,Vatin Vincent,Balkau Beverley,Lantieri Olivier,Raverdy Violeta,Pattou François,Van Hul Wim,Van Gaal Luc,Peet Daniel J.,Weill Jacques,Miller Jennifer L.,Horber Fritz,Goldstone Anthony P.,Driscoll Daniel J.,Bruning John B.,Meyre David,Whitelaw Murray L.,Froguel Philippe

Publisher

American Society for Clinical Investigation

Subject

General Medicine

Reference17 articles.

1. Development of neuroendocrine lineages requires the bHLH–PAS transcription factor SIM1

2. Sim1 haploinsufficiency causes hyperphagia, obesity and reduction of the paraventricular nucleus of the hypothalamus

3. Sim1 gene dosage modulates the homeostatic feeding response to increased dietary fat in mice

4. Adenoviral-Mediated Modulation of Sim1 Expression in the Paraventricular Nucleus Affects Food Intake

5. Interstitial 6q deletion with a Prader--Willi-like phenotype: a new case and review of the literature

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