{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,16]],"date-time":"2026-10-16T22:39:46Z","timestamp":1792190386990,"version":"4.4.0"},"reference-count":1,"publisher":"Springer Science and Business Media LLC","issue":"6629","license":[{"start":{"date-parts":[[1997,5,1]],"date-time":"1997-05-01T00:00:00Z","timestamp":862444800000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.springer.com\/tdm"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Nature"],"published-print":{"date-parts":[[1997,5]]},"DOI":"10.1038\/387151a0","type":"journal-article","created":{"date-parts":[[2003,8,11]],"date-time":"2003-08-11T22:28:06Z","timestamp":1060640886000},"page":"151-158","source":"Crossref","is-referenced-by-count":619,"title":["Altered cell differentiation and proliferation in mice lacking p57KIP2 indicates a role in Beckwith\u2013Wiedemann syndrome"],"prefix":"10.1038","volume":"387","author":[{"given":"Pumin","family":"Zhang","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nanette J.","family":"Li\u00e9geois","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Calvin","family":"Wong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Milton","family":"Finegold","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harry","family":"Hou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janet C.","family":"Thompson","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adam","family":"Silverman","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. Wade","family":"Harper","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ronald A.","family":"DePinho","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen J.","family":"Elledge","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","reference":[{"key":"BF387151a0_CR1","doi-asserted-by":"crossref","unstructured":"1. Harper, J. W. & Elledge, S. J. Cdk inhibitors in development and cancer. Curr. Opin. Genet. Dev. 6,56-64 (1996). 2. Sherr, C. J. Cancer cell cycles. Science 274, 1672-1677 (1996). 3. Weinberg, R. A. The retinoblastoma protein and cell cycle control. Cell 81, 323-330 (1995). 4. Serrano, M. et al. Role of the INK4a locus in tumor suppression and cell mortality. Cell 85, 27-37 (1996). 5. Parker, S. B. et al. p53-Independent expression of p21Clpl in muscle and other terminally differentiating cells. Science 267, 1024-1027 (1995). 6. Deng, C. et al. Mice lacking p2iapl\/WAF1 undergo normal development, but are defective in Gl checkpoint control. Cell 82, 675-684 (1995). 7. Nakayama, K. et al. Mice lacking p27KIP1 display increased body size, multiple organ hyperplasia, retinal displasia, and pituitary tumors. Cell 85, 707-720 (1996). 8. Kiyokawa, H. et al. Enhanced growth of mice lacking the cyclin-dependent kinase inhibitor function of p27KIP1. Cell 85, 721-732 (1996). 9. Fero, M. L. et al. A syndrome of multiorgan hyperplasia with features of gigantism, tumorigenesis, and female sterility in p27Kipl-deficient mice. Cell 85, 733-744 (1996). 10. Matsuoka, S. et al. p57KIP2, a structurally distinct member of the p21CIP1 Cdk-inhibitor family, is a candidate tumor suppressor gene. Genes Dev. 9, 650-662 (1995). 11. Lee, M. L. etal. Cloning of p57KIP2, a cyclin-dependent kinase inhibitor with unique domain structure and tissue distribution. Genes Dev. 9, 639-649 (1995). 12. Hastie, N. D. The genetics of Wilms' tumor-a case of disrupted development. Annu. Rev. Genet. 28, 523-558 (1994). 13. Wiedemann, H. R. Tumours and hemihypertrophy associated with Wiedemann-Beckwith syndrome. Eur. J. Pediatr. 141, 129-134 (1983). 14. Junien, C. Beckwith-Wiedemann syndrome, tumourigenesis and imprinting. Curr. Opin. Biol. 2, 431-438 (1992). 15. Matsuoka, S. et al. Imprinting of the gene encoding a human cyclin-dependent kinase inhibitor p57rap2, on chromosome llplS. Proc. Natl Acad. Sci. USA 93, 3026-3030 (1996). 16. Hatada, I. & Mukai, T. Genomic imprinting of p57KIP2, a cyclin-dependent kinase inhibitor, in mouse. Nature Genet. 11, 204-206 (1995). 17. Hoovers, J. et al Multiple genetic loci within Ilpl5.5 denned by Beckwith-Wiedemann Syndrome rearrangement breakpoints and subchromosomal transferable fragments. Proc. Natl Acad. Sci. USA 92, 12456-12460 (1995). 18. Hatada, I. et al An imprinted gene p57KIP2 is mutated in Beckwith-Wiedemann syndrome. Nature Genet. 14, 171-173 (1996). 19. Kaufman, M. H. The Atlas of Mouse Development (Academic, London, 1992). 20. Ferguson, M. J. W. Palate development. Development (suppl.) 103, 41-60 (1988). 21. Beckwith, B. Macroglossia, omphalocele, adrenal cytomegaly, gigantism, and hyperplastic visceromegaly. Birth Defects: Original Article Series 2 Vol. V No. 2 (ed. Bergsma, D.) 188-196 (The National Foundation, 1969). 22. Hepinstall, R. H. in Pathology of the Kidney Vol. 1, 114-155 (Little, Brown, Boston, MA, 1992). 23. Jacenko, O. et al. Spondylometaphyseal dysplasia in mice carrying a dominant negative mutation in a matrix protein specific for cartilage-to-bone transition. Nature 365, 56-61 (1993). 24. McAvoy, J. W. Induction of the eye lens. Differentiation 17, 137-149 (1996). 25. Morgenbesser, S. D. et al. p53-dependent apoptosis produced by Rb deficiency in the developing mouse lens. Nature 371, 72-74 (1994). 26. Cobrink, D. et al. Shared role of the Rb-related p!30 and p!07 proteins in limb development. Genes Dev. 10, 1633-1644 (1996). 27. Elliott, M. et al. Clinical features and natural history of Beckwith-Wiedemann syndrome: presentation of 74 new cases. Clin. Genet. 46, 168-174 (1994). 28. Takato, T., Kamei, M., Kato, K. & Kitano, I. Cleft palate in the Beckwith-Wiedemann syndrome. Ann. Plastic Surg. 22, 347-349 (1989). 29. Sotelo-Avila, C., Gonzalez-Crussi, F. & Fowler, J. W. Complete and incomplete forms of Beckwith-Wiedemann syndrome: their oncogenic potential\/. Pediatr. 96, 47-50 (1980). 30. Leighton, P. A. et al Disruption of imprinting caused by deletion of the H19 gene region in mice. Nature 375, 34-39 (1995). 31. Weksberg, R., Shem, D. R., Song, Q. L. & Squire, J, Disruption of IGF2 imprinting in Beckwith-Wiedemann Syndrome. Nature Genet. 5, 143-149 (1993). 32. Ramirez-Solis, R. et al. Hoxb-4 (Hox-2.6) mutant mice show homeotic transformation of a cervical vertebra and defects in the closure of the sternal rudiments. Cell 73, 279-294 (1993). 33. Dynlacht, B. D. et al. Purification and analysis of CIP\/KIP proteins. Methods Enzymol. (in the press).","DOI":"10.1016\/S0959-437X(96)90011-8"}],"container-title":["Nature"],"original-title":[],"language":"en","link":[{"URL":"http:\/\/www.nature.com\/articles\/387151a0","content-type":"text\/html","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/www.nature.com\/articles\/387151a0.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"text-mining"},{"URL":"http:\/\/www.nature.com\/articles\/387151a0.pdf","content-type":"application\/pdf","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,5,17]],"date-time":"2023-05-17T20:10:25Z","timestamp":1684354225000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.nature.com\/articles\/387151a0"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1997,5]]},"references-count":1,"journal-issue":{"issue":"6629","published-print":{"date-parts":[[1997,5]]}},"alternative-id":["BF387151a0"],"URL":"https:\/\/doi.org\/10.1038\/387151a0","relation":{},"ISSN":["0028-0836","1476-4687"],"issn-type":[{"value":"0028-0836","type":"print"},{"value":"1476-4687","type":"electronic"}],"subject":[],"published":{"date-parts":[[1997,5]]}}}