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

Pumin Zhang, Nanette J. Liégeois, Calvin Wong, Milton Finegold, Harry Hou, Janet C. Thompson, Adam Silverman, J. Wade Harper, Ronald A. DePinho and Stephen J. Elledge
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Pumin Zhang: Baylor College of Medicine
Nanette J. Liégeois: Albert Einstein College of Medicine
Calvin Wong: Baylor College of Medicine
Milton Finegold: and Baylor College of Medicine
Harry Hou: Albert Einstein College of Medicine
Janet C. Thompson: Baylor College of Medicine
Adam Silverman: Albert Einstein College of Medicine
J. Wade Harper: Baylor College of Medicine
Ronald A. DePinho: Albert Einstein College of Medicine
Stephen J. Elledge: Baylor College of Medicine

Nature, 1997, vol. 387, issue 6629, 151-158

Abstract: 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.

Date: 1997
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DOI: 10.1038/387151a0

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