Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Magel2 knockout mice manifest altered social phenotypes and a deficit in preference for social novelty.

Genes, brain, and behavior - 1 Jul 2017

Fountain M D, Tao H, Chen C-A, Yin J, Schaaf C P

Abstract excerpt

MAGEL2 is one of five protein-coding, maternally imprinted, paternally expressed genes in the Prader-Willi syndrome (PWS)-critical domain on chromosome 15q11-q13. Truncating pathogenic variants of MAGEL2 cause Schaaf-Yang syndrome (SHFYNG) (OMIM #615547), a neurodevelopmental disorder related to PWS. Affected individuals manifest a spectrum of neurocognitive and behavioral phenotypes, including intellectual...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Antigens, Neoplasm
Share to Exploratory Behavior
Share to Mice

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Mice, Inbred C57BL

Share to Phenotype

Share to Prader-Willi Syndrome

Share to Proteins

Share to Social Behavior

Source

Open in PubMed Open full text

Identifiers

PMID: 28296079
DOI: 10.1111/gbb.12378
PMCID: PMC5495607

Genes

MAGEL2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 2 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Magel2 knockout mice manifest altered social phenotypes and a deficit in preference for social novelty.PMID 28296079Read ↗

In-depth behavioral characterization of a rat model of Schaaf-Yang syndromeSemantic 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 ↗

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

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

Two mouse models carrying truncating mutations in Magel2 show distinct phenotypes.Semantic proximity Read ↗

Behavioral Phenotyping of an Improved Mouse Model of Phelan-McDermid Syndrome with a Complete Deletion of the Shank3 Gene.Semantic proximity Read ↗

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

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

The adult phenotype of Schaaf-Yang syndrome.Semantic proximity Read ↗

Behavioural characteristics of the Prader-Willi syndrome related biallelic Snord116 mouse model.Semantic proximity Read ↗

Investigation of a Novel Mouse Model of Prader-Willi Syndrome with Invalidation of <i>Necdin</i> and <i>Magel2</i>Semantic proximity Read ↗

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

⌁Select a neighboring publication to make it the new centre.