Leptin signaling defects in a mouse model of Prader-Willi syndrome: An orphan genetic obesity syndrome no more?
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Prader-Willi and Angelman SyndromeThe Prader-Willi syndrome proteins MAGEL2 and necdin regulate leptin receptor cell surface abundance through ubiquitination pathways.Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome.
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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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article científic
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article scientifique
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bilimsel makale
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scientific article published on 27 March 2013
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vedecký článok
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name
Leptin signaling defects in a ...... etic obesity syndrome no more?
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Leptin signaling defects in a ...... etic obesity syndrome no more?
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Leptin signaling defects in a ...... etic obesity syndrome no more?
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Leptin signaling defects in a ...... etic obesity syndrome no more?
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Leptin signaling defects in a ...... etic obesity syndrome no more?
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Leptin signaling defects in a ...... etic obesity syndrome no more?
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Leptin signaling defects in a ...... etic obesity syndrome no more?
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William F Colmers
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P304
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10.4161/RDIS.24421
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2013-03-27T00:00:00Z