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Characterizing the Mesolimbic Dopamine Reward Pathway in a Magel2-null Mouse, a Model of Prader-Willi Syndrome
DownloadFall 2016
Prader-Willi Syndrome (PWS) is a genetic disorder characterized by extreme hyperphagia that can lead to severe obesity. The abnormal motivation to eat in PWS suggests a disruption in the hedonic feeding pathway, which is feeding based on reward as opposed to physiological need. Hedonic feeding is...
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Inactivation of Magel2 in a mouse model of Prader-Willi Syndrome alters autophagy in the hypothalamus and impairs muscle function
DownloadFall 2016
Prader-Willi Syndrome (PWS) is a neurodevelopmental disorder causing severe neonatal hypotonia that persists until adulthood, reduced muscle mass, and hyperphagia leading to childhood-onset obesity. PWS is caused by inactivation of several genes located on chromosome 15q11-q13, including MAGEL2....
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Investigation of the Prader-Willi syndrome protein MAGEL2 in the regulation of Forkhead box transcription factor FOXO1
DownloadSpring 2013
Prader-Willi syndrome (PWS), a genetic disorder resulting from the loss of expression of multiple genes including MAGEL2, is characterized by hyperphagia and childhood-onset obesity. These symptoms point to dysfunction in the regulation of energy homeostasis. Magel2 is highly expressed in the...
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MAGEL2 regulates leptin receptor internalization through ubiquitination pathways involving USP8 and RNF41
DownloadSpring 2017
Children with Prader-Willi syndrome have neonatal feeding difficulties, developmental delay and excessive appetite. Loss of MAGEL2 alone causes a related neurodevelopmental disorder (Schaaf-Yang syndrome) and may contribute to obesity in children with Prader-Willi syndrome who lack MAGEL2 and...