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Journal Abstract Search

326 related items for PubMed ID: 28973533

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  • 2. Progressive postnatal decline in leptin sensitivity of arcuate hypothalamic neurons in the Magel2-null mouse model of Prader-Willi syndrome.
    Pravdivyi I, Ballanyi K, Colmers WF, Wevrick R.
    Hum Mol Genet; 2015 Aug 01; 24(15):4276-83. PubMed ID: 25926624
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  • 3. Magel2 is required for leptin-mediated depolarization of POMC neurons in the hypothalamic arcuate nucleus in mice.
    Mercer RE, Michaelson SD, Chee MJ, Atallah TA, Wevrick R, Colmers WF.
    PLoS Genet; 2013 Aug 01; 9(1):e1003207. PubMed ID: 23341784
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  • 4. Essential role for the Prader-Willi syndrome protein necdin in axonal outgrowth.
    Lee S, Walker CL, Karten B, Kuny SL, Tennese AA, O'Neill MA, Wevrick R.
    Hum Mol Genet; 2005 Mar 01; 14(5):627-37. PubMed ID: 15649943
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  • 10. Necdin, a Prader-Willi syndrome candidate gene, regulates gonadotropin-releasing hormone neurons during development.
    Miller NL, Wevrick R, Mellon PL.
    Hum Mol Genet; 2009 Jan 15; 18(2):248-60. PubMed ID: 18930956
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  • 12. Expression and imprinting of MAGEL2 suggest a role in Prader-willi syndrome and the homologous murine imprinting phenotype.
    Lee S, Kozlov S, Hernandez L, Chamberlain SJ, Brannan CI, Stewart CL, Wevrick R.
    Hum Mol Genet; 2000 Jul 22; 9(12):1813-9. PubMed ID: 10915770
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  • 15. Necdin-related MAGE proteins differentially interact with the E2F1 transcription factor and the p75 neurotrophin receptor.
    Kuwako K, Taniura H, Yoshikawa K.
    J Biol Chem; 2004 Jan 16; 279(3):1703-12. PubMed ID: 14593116
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