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Article

Oppositely imprinted genes p57(Kip2) and igf2 interact in a mouse model for Beckwith-Wiedemann syndrome.

Genes & development - 1 Dec 1999

Caspary T, Cleary M A, Perlman E J, Zhang P, Elledge S J, Tilghman S M

Abstract excerpt

Beckwith-Wiedemann syndrome (BWS) is a clinically variable disorder characterized by somatic overgrowth, macroglossia, abdominal wall defects, visceromegaly, and an increased susceptibility to childhood tumors. The disease has been linked to a large cluster of imprinted genes at human chromosome 11p15.5. A subset of BWS patients has been identified with loss-of-function mutations in p57(KIP2), a maternally...

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Identifiers

PMID: 10601037
DOI: 10.1101/gad.13.23.3115
PMCID: PMC317182

Genes

IGF2

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-08.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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Oppositely imprinted genes p57(Kip2) and igf2 interact in a mouse model for Beckwith-Wiedemann syndrome.PMID 10601037Read ↗

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