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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...
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Fall 2010
Prader-Willi syndrome (PWS) is a rare, neurodevelopmental disorder with multiple features caused by hypothalamic deficiency, including infantile failure to thrive, hyperphagia leading to obesity, growth hormone deficiency, hypogonadism, and central adrenal insufficiency. Other features of PWS...
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The role of the Prader-Willi syndrome obesity protein, MAGEL2 in the proper functioning of circadian rhythm
DownloadFall 2010
MAGEL2 is one of the five genes inactivated in Prader-Willi Syndrome (PWS), a genetic disorder, manifesting with symptoms of developmental delay and morbid obesity. Magel2 is highly expressed in the suprachiasmatic nucleus, which is the location of the central clock or circadian pacemaker. Magel2...