Discover Community Create You

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

Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndrome

27 Jun 2007

Abstract excerpt

Prader-Willi syndrome (PWS) is an imprinted genetic obesity disorder characterized by abnormalities of growth and metabolism. Multiple mouse models with deficiency of one or more PWS candidate genes have partially correlated individual genes with aspects of the PWS phenotype, although the genetic origin of defects in growth and metabolism has not been elucidated. Gene-targeted mutation of the PWS candidate gene...

Read the complete abstract on PubMed

Topics

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

Share to Genetic Syndromes and Imprinting
Share to Genetics and Neurodevelopmental Disorders
Share to Pancreatic function and diabetes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 17728320
DOI: 10.1093/hmg/ddm225

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 6 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Inactivation of the mouse Magel2 gene results in growth abnormalities similar to Prader-Willi syndromePMID 17728320Read ↗

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

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

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

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

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

Loss of Magel2 impairs the development of hypothalamic Anorexigenic circuitsSemantic 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 ↗

Muscle dysfunction caused by loss of<i>Magel2</i>in a mouse model of Prader-Willi and Schaaf-Yang syndromesSemantic proximity Read ↗

<i>Magel2</i> in hypothalamic POMC neurons influences the impact of stress on anxiety-like behavior and spatial learning associated with a food reward in male miceSemantic proximity Read ↗

Disruption of the Igf2 gene alters hepatic lipid homeostasis and gene expression in the newborn mouse.Semantic proximity Read ↗

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

Impaired hypothalamic regulation of endocrine function and delayed counterregulatory response to hypoglycemia in Magel2-null mice.Semantic proximity Read ↗

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