Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith–Wiedemann syndrome
- 1 May 1997
- journal article
- Published by Springer Nature in Nature
- Vol. 387 (6629) , 151-158
- https://doi.org/10.1038/387151a0
Abstract
Mice lacking the imprinted Cdk inhibitor p57(KIP2) 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 p57(KIP2) expression may play a role in the condition.Keywords
This publication has 1 reference indexed in Scilit:
- Cdk inhibitors in development and cancerCurrent Opinion in Genetics & Development, 1996