Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith–Wiedemann syndrome View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-05

AUTHORS

Pumin Zhang, Nanette J. Liégeois, Calvin Wong, Milton Finegold, Harry Hou, Janet C. Thompson, Adam Silverman, J. Wade Harper, Ronald A. DePinho, Stephen J. Elledge

ABSTRACT

Mice lacking the imprinted Cdk inhibitor p57KIP2 have altered cell proliferation and differentiation, leading to abdominal muscle defects; cleft palate; endochondral bone ossification defects with incomplete differentiation of hypertrophic chondrocytes; renal medullary dysplasia; adrenal cortical hyperplasia and cytomegaly; and lens cell hyperproliferation and apoptosis. Many of these phenotypes are also seen in patients with Beckwith–Wiedemann syndrome, a pleiotropic hereditary disorder characterized by overgrowth and predisposition to cancer, suggesting that loss of p57KIP2 expression may play a role in the condition. More... »

PAGES

151-158

Journal

TITLE

Nature

ISSUE

6629

VOLUME

387

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/387151a0

DOI

http://dx.doi.org/10.1038/387151a0

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1045568530

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/9144284


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