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Article

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

Human molecular genetics - 22 Jul 2000

Lee S, Kozlov S, Hernandez L, Chamberlain S J, Brannan C I, Stewart C L, Wevrick R

Abstract excerpt

Prader-Willi syndrome (PWS) is caused by the loss of expression of imprinted genes in chromosome 15q11-q13. Affected individuals exhibit neonatal hypotonia, developmental delay and childhood-onset obesity. Necdin, a protein implicated in the terminal differentiation of neurons, is the only PWS candidate gene to reduce viability when disrupted in a mouse model. In this study, we have characterized MAGEL2 (also...

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Source

Identifiers

PMID: 10915770
DOI: 10.1093/hmg/9.12.1813

Genes

MAGEL2
NDN

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

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Click a neighbor to travelStep 1 · 12 closest

Expression and imprinting of MAGEL2 suggest a role in Prader-willi syndrome and the homologous murine imprinting phenotype.PMID 10915770Read ↗

A necdin/MAGE-like gene in the chromosome 15 autism susceptibility region: expression, imprinting, and mapping of the human and mouse orthologues.Semantic proximity Read ↗

The Necdin Gene is Deleted in Prader-Willi Syndrome and is Imprinted in Human and MouseSemantic proximity Read ↗

The mouse Necdin gene is expressed from the paternal allele only and lies in the 7C region of the mouse chromosome 7, a region of conserved synteny to the human Prader-Willi syndrome region.Semantic proximity Read ↗

Disruption of the mouse necdin gene results in early post-natal lethality.Semantic proximity Read ↗

The human necdin gene, NDN, is maternally imprinted and located in the Prader-Willi syndrome chromosomal regionSemantic proximity Read ↗

Necdin, a Prader-Willi syndrome candidate gene, regulates gonadotropin-releasing hormone neurons during developmentSemantic 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 ↗

Placental defects revealed by modelling PWS in miceSemantic proximity Read ↗

Prader-Willi syndrome transcripts are expressed in phenotypically significant regions of the developing mouse brain.Semantic proximity Read ↗

A Case of Prader-Willi Syndrome With a Deletion Including MAGEL2 , NDN , and MKRN3 , but Excluding SNRPN and SNORD116.Semantic proximity Read ↗

Loss of the Prader-Willi syndrome protein necdin causes defective migration, axonal outgrowth, and survival of embryonic sympathetic neurons.Semantic proximity Read ↗

Paternal deletion from Snrpn to Ube3a in the mouse causes hypotonia, growth retardation and partial lethality and provides evidence for a gene contributing to Prader-Willi syndrome.Semantic proximity Read ↗

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