| First Author | Takahashi K | Year | 2000 |
| Journal | J Biochem | Volume | 127 |
| Issue | 1 | Pages | 73-83 |
| PubMed ID | 10731669 | Mgi Jnum | J:61190 |
| Mgi Id | MGI:1354550 | Doi | 10.1093/oxfordjournals.jbchem.a022586 |
| Citation | Takahashi K, et al. (2000) Mice lacking a CDK inhibitor, p57(Kip2), exhibit skeletal abnormalities and growth retardation. J Biochem 127(1):73-83 |
| abstractText | p57(Kip2), one of the cyclin-dependent kinase (CDK) inhibitors, has been suggested to be a tumor suppressor candidate. To elucidate its biological roles in mouse development and tumorigenesis, we created p57(Kip2)-deficient mice. The p57(Kip2)-deficient mice exhibited a cleft palate and defective bone formation resulting in severe dyspnea. Most of the p57(Kip2)-deficient mice died within 24 h after birth, while about 10% of them survived beyond the weaning period. All of the surviving mice showed severe growth retardation. The males showed immaturity of the testes, prostate and seminal vesicles, and the females showed vaginal atresia, immaturity of the uterus, and an increased number of atretic follicles. Although Yan et al. and Zhang et al. have already reported p57(Kip2)-deficient mice, they could not investigate the phenotypes of the surviving p57(Kip2)-deficient mice. Also, most of the symptoms of Beckwith-Wiedemann syndrome could not be reproduced in the mutant mice. Embryonic fibroblasts prepared from p57(Kip2)-deficient mice showed no differences in the proliferation rate and saturation density, suggesting that G1 arrest is largely independent of p57(Kip2) function. Our results suggest that p57(Kip2) plays a critical role in development, but do not support the hypothesis that the p57(Kip2) gene is a tumor-suppressor gene or is responsible for Beckwith-Wiedemann syndrome. |
