Loss of Magel2 impairs the development of hypothalamic Anorexigenic circuits-Reference-Cited by-同舟云学术

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Loss of Magel2 impairs the development of hypothalamic Anorexigenic circuits

Published:2016-06-10 Issue:15 Volume:25 Page:3208-3215
ISSN:0964-6906
Container-title:Human Molecular Genetics
language:en
Short-container-title:Hum. Mol. Genet.

Author:

Maillard Julien,Park Soyoung,Croizier Sophie,Vanacker Charlotte,Cook Joshua H.,Prevot Vincent,Tauber Maithe,Bouret Sebastien G.

Publisher

Oxford University Press (OUP)

Subject

Genetics (clinical),Genetics,Molecular Biology,General Medicine

Reference47 articles.

1. The role of genomic imprinting in human developmental disorders: lessons from Prader-Willi syndrome

2. Expression and imprinting of MAGEL2 suggest a role in Prader-Willi syndrome and the homologous murine imprinting phenotype

3. Prader–Willi syndrome transcripts are expressed in phenotypically significant regions of the developing mouse brain

4. The imprinted gene Magel2 regulates normal circadian output

5. Distributed Neural Control of Energy Balance: Contributions from Hindbrain and Hypothalamus

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1. Investigation of a Novel Mouse Model of Prader-Willi Syndrome with Invalidation ofNecdinandMagel2;2024-07-24

2. MAGEL2 (patho‐)physiology and Schaaf–Yang syndrome;Developmental Medicine & Child Neurology;2024-07

3. AAV-BDNF gene therapy ameliorates a hypothalamic neuroinflammatory signature in the Magel2-null model of Prader-Willi syndrome;Molecular Therapy - Methods & Clinical Development;2023-12

4. Food socialization of children with Prader-Willi syndrome: an interdisciplinary problematization;Frontiers in Nutrition;2023-06-06

5. Current Treatments for Patients with Genetic Obesity;Journal of Clinical Research in Pediatric Endocrinology;2023-05-29

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