Magel2 is required for leptin-mediated depolarization of POMC neurons in the hypothalamic arcuate nucleus in mice (Q28485151)

1

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Sheldon D Michaelson

2

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Melissa J S Chee

3

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Tanya A Atallah

4

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Rachel Wevrick

5

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William F Colmers

Creative Commons Attribution 4.0 International

6

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language of work or name

English

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publication date

2013

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published in

PLOS Genetics

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volume

9

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issue

1

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page(s)

e1003207

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copyright license

start time

17 January 2013

1 reference

April 2022 Public Data File from Crossref

copyright status

copyrighted

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Unabated anorexic and enhanced thermogenic responses to melanotan II in diet-induced obese rats despite reduced melanocortin 3 and 4 receptor expression

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The imprinted gene Magel2 regulates normal circadian output

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Differential mechanisms and development of leptin resistance in A/J versus C57BL/6J mice during diet-induced obesity

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

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Leptin directly activates SF1 neurons in the VMH, and this action by leptin is required for normal body-weight homeostasis

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Heterozygosity for aPOMC-Null Mutation and Increased Obesity Risk in Humans

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12 December 2020

Leptin activates neurons in ventrobasal hypothalamus and brainstem

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Obesity in the mouse model of pro-opiomelanocortin deficiency responds to peripheral melanocortin

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A single postnatal injection of oxytocin rescues the lethal feeding behaviour in mouse newborns deficient for the imprinted Magel2 gene

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Nociceptin/orphanin FQ suppresses the excitability of neurons in the ventromedial nucleus of the hypothalamus

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12 December 2020

10.1371/JOURNAL.PGEN.1003207

Identifiers

DOI

1 reference

1 reference

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PubMed publication ID

23341784

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