| First Author | Swanger WJ | Year | 1997 |
| Journal | Bioessays | Volume | 19 |
| Issue | 10 | Pages | 839-42 |
| PubMed ID | 9363677 | Mgi Jnum | J:44138 |
| Mgi Id | MGI:1099390 | Doi | 10.1002/bies.950191002 |
| Citation | Swanger WJ, et al. (1997) p57KIP2 targeted disruption and Beckwith-Wiedemann syndrome: is the inhibitor just a contributor?. Bioessays 19(10):839-42 |
| abstractText | Beckwith-Wiedemann syndrome is a human congenital disorder characterized by a wide variety of growth abnormalities, including developmental defects and predisposition to certain tumors. Genetic evidence has suggested a role for p57KIP2, a member of a family of cell cycle inhibitory genes, in Beckwith-Wiedemann syndrome. Two independent groups have reported the generation and characterization of mice lacking functional p57KIP2. These mice demonstrate a number of abnormal phenotypes which overlap with, although do not completely recapitulate, Beckwith-Wiedemann syndrome. These findings advance the molecular characterization of a human disorder, and provide insight into the interplay between regulation of cell division and development. |
