ArticlePloS one2009
Loss of magel2, a candidate gene for features of Prader-Willi syndrome, impairs reproductive function in mice.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
52 citing papers in PubMed, 2 syntheses or guidelines pooled it, 99 citations in OpenAlex.
- A systematic-review of olfactory deficits in neurodevelopmental disorders: From mouse to human.Neuroscience and biobehavioral reviews · 2021Pooled it
- Recommendations for the investigation of animal models of Prader-Willi syndrome.Mammalian genome : official journal of the International Mammalian Genome Society · 2013Guideline
- SMCHD1 is a target for gene activation therapy to treat Prader-Willi syndrome.Science advances · 2026Article
- Article
- Mom genes and dad genes: genomic imprinting in the regulation of social behaviors.Epigenomics · 2025Review
- MAGEL2 (patho-)physiology and Schaaf-Yang syndrome.Developmental medicine and child neurology · 2025Review
- Article
- Assessment of inbreeding coefficients and inbreeding depression on complex traits from genomic and pedigree data in Nelore cattle.BMC genomics · 2024Article
- Characterization of Circulating Protein Profiles in Individuals with Prader-Willi Syndrome and Individuals with Non-Syndromic Obesity.Journal of clinical medicine · 2024Article
- Illuminating the terminal nerve: Uncovering the link between GnRH-1 neuron and olfactory development.The Journal of comparative neurology · 2024Article
- Endocrine features of Prader-Willi syndrome: a narrative review focusing on genotype-phenotype correlation.Frontiers in endocrinology · 2024Review
- Hormonal Imbalances in Prader-Willi and Schaaf-Yang Syndromes Imply the Evolution of Specific Regulation of Hypothalamic Neuroendocrine Function in Mammals.International journal of molecular sciences · 2023Review
- Early onset critically ill infants with Schaaf-Yang syndrome: a retrospective study from the China neonatal genomes project and literature review.Annals of translational medicine · 2023Article
- Preimplantation Genetic Testing (PGT) and Prenatal Diagnosis of Schaaf-Yang Syndrome: A Report of Three Families and a Research on Genotype-Phenotype Correlations.Journal of clinical medicine · 2023Article
- Linking oxytocin and arginine vasopressin signaling abnormalities to social behavior impairments in Prader-Willi syndrome.Neuroscience and biobehavioral reviews · 2022Review
- Article
- Novel genes and variants associated with congenital pituitary hormone deficiency in the era of next-generation sequencing.Frontiers in endocrinology · 2022Review
- From leptin to lasers: the past and present of mouse models of obesity.Expert opinion on drug discovery · 2021Article
- A Comprehensive Review of Genetically Engineered Mouse Models for Prader-Willi Syndrome Research.International journal of molecular sciences · 2021Review
- Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMAGEL2 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 increased adiposity after weaning. PRINCIPAL
findingsWe now show that loss of Magel2 in mice causes reduced fertility in both males and females through extended breeding intervals and early reproductive decline and termination. Female Magel2-null mice display extended and irregular estrous cycles, while males show decreased testosterone levels, and reduced olfactory preference for female odors.
conclusionsOur results suggest that loss of MAGEL2 contributes to the reproductive deficits seen in people with PWS, and further highlights the role of normal circadian rhythm in the maintenance of fertility.
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Registered trials
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