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Article

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

PloS one - 1 Jan 2009

Mercer Rebecca E, Wevrick Rachel

Abstract excerpt

BACKGROUND: MAGEL2 is one of several genes typically inactivated in the developmental obesity disorder Prader-Willi syndrome (PWS). The physiological consequences of loss of MAGEL2, but without the concurrent loss of other PWS genes, are not well understood. Gene-targeted mutation of Magel2 in mice disrupts circadian rhythm and metabolism causing reduced total activity, reduced weight gain before weaning, and...

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Source

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Identifiers

PMID: 19172181
DOI: 10.1371/journal.pone.0004291
PMCID: PMC2627930

Genes

MAGEL2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026. Manifest publication-graph-cohort-2026-09-06.1.

Source receipt: pubmed, retrieved 6 Sept 2026.

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Loss of magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice.PMID 19172181Read ↗

Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndromeSemantic proximity Read ↗

The imprinted gene Magel2 regulates normal circadian output.Semantic proximity Read ↗

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Hormonal Imbalances in Prader–Willi and Schaaf–Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in MammalsSemantic proximity Read ↗

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Prader-Willi syndrome: advances in genetics, pathophysiology and treatment.Semantic proximity Read ↗

A truncating mutation of <i>Magel2</i> in the rat modelled for the study of Schaaf-Yang and Prader-Willi syndromes alters select behavioral and physiological outcomesSemantic proximity Read ↗

Magel2 truncation alters select behavioral and physiological outcomes in a rat model of Schaaf-Yang syndrome.Semantic proximity Read ↗

Hormonal and Metabolic Defects in a Prader-Willi Syndrome Mouse Model with Neonatal Failure to ThriveSemantic proximity Read ↗

Magel2 deficiency promotes cardiac remodeling and increases arrhythmogenic susceptibility in a mouse model relevant to Prader-Willi and Schaaf-Yang syndromes.Semantic proximity Read ↗

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