| First Author | Zhang P | Year | 1997 |
| Journal | Nature | Volume | 387 |
| Issue | 6629 | Pages | 151-8 |
| PubMed ID | 9144284 | Mgi Jnum | J:40203 |
| Mgi Id | MGI:87545 | Doi | 10.1038/387151a0 |
| Citation | Zhang P, et al. (1997) Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith-Wiedemann syndrome. Nature 387(6629):151-8 |
| abstractText | 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. |
