Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome (Q48201315)

9 February 2018

title

Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome (English)

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author

Rachel Wevrick

4

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author name string

Igor Pravdivyi

1

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Klaus Ballanyi

2

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William F Colmers

3

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publication date

29 April 2015

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published in

Human Molecular Genetics

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volume

24

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issue

15

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page(s)

4276-4283

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Nutritional phases in Prader-Willi syndrome.

cites work

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Magel2 is required for leptin-mediated depolarization of POMC neurons in the hypothalamic arcuate nucleus in mice

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Leptin signaling defects in a mouse model of Prader-Willi syndrome: An orphan genetic obesity syndrome no more?

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The human MAGEL2 gene and its mouse homologue are paternally expressed and mapped to the Prader-Willi region

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The imprinted gene Magel2 regulates normal circadian output

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Loss of magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice

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Leptin receptor signaling in POMC neurons is required for normal body weight homeostasis

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VPS35 Parkinson mutation impairs autophagy via WASH.

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Identifiers

DOI

10.1093/HMG/DDV159

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9 February 2018

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9 February 2018