| pubmed-article:7664346 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7664346 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:7664346 | lifeskim:mentions | umls-concept:C1821244 | lld:lifeskim |
| pubmed-article:7664346 | lifeskim:mentions | umls-concept:C0249197 | lld:lifeskim |
| pubmed-article:7664346 | lifeskim:mentions | umls-concept:C1749568 | lld:lifeskim |
| pubmed-article:7664346 | lifeskim:mentions | umls-concept:C2587213 | lld:lifeskim |
| pubmed-article:7664346 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:7664346 | pubmed:dateCreated | 1995-10-6 | lld:pubmed |
| pubmed-article:7664346 | pubmed:abstractText | p21CIP1/WAF1 is a CDK inhibitor regulated by the tumor suppressor p53 and is hypothesized to mediate G1 arrest. p53 has been suggested to derive anti-oncogenic properties from this relationship. To test these notions, we created mice lacking p21CIP1/WAF1. They develop normally and (unlike p53-/- mice) have not developed spontaneous malignancies during 7 months of observation. Nonetheless, p21-/- embryonic fibroblasts are significantly deficient in their ability to arrest in G1 in response to DNA damage and nucleotide pool perturbation. p21-/- cells also exhibit a significant growth alteration in vitro, achieving a saturation density as high as that observed in p53-/- cells. In contrast, other aspects of p53 function, such as thymocytic apoptosis and the mitotic spindle checkpoint, appear normal. These results establish the role of p21CIP1/WAF1 in the G1 checkpoint, but suggest that the anti-apoptotic and the anti-oncogenic effects of p53 are more complex. | lld:pubmed |
| pubmed-article:7664346 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7664346 | pubmed:language | eng | lld:pubmed |
| pubmed-article:7664346 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:7664346 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:7664346 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:7664346 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:7664346 | pubmed:issn | 0092-8674 | lld:pubmed |
| pubmed-article:7664346 | pubmed:author | pubmed-author:HarperJ WJW | lld:pubmed |
| pubmed-article:7664346 | pubmed:author | pubmed-author:LederPP | lld:pubmed |
| pubmed-article:7664346 | pubmed:author | pubmed-author:DenkGG | lld:pubmed |
| pubmed-article:7664346 | pubmed:author | pubmed-author:ZhangPP | lld:pubmed |
| pubmed-article:7664346 | pubmed:author | pubmed-author:ElledgeS JSJ | lld:pubmed |
| pubmed-article:7664346 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:7664346 | pubmed:day | 25 | lld:pubmed |
| pubmed-article:7664346 | pubmed:volume | 82 | lld:pubmed |
| pubmed-article:7664346 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:7664346 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:7664346 | pubmed:pagination | 675-84 | lld:pubmed |
| pubmed-article:7664346 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:7664346 | pubmed:meshHeading | pubmed-meshheading:7664346-... | lld:pubmed |
| pubmed-article:7664346 | pubmed:year | 1995 | lld:pubmed |
| pubmed-article:7664346 | pubmed:articleTitle | Mice lacking p21CIP1/WAF1 undergo normal development, but are defective in G1 checkpoint control. | lld:pubmed |
| pubmed-article:7664346 | pubmed:affiliation | Howard Hughes Medical Institute, Department of Genetics, Harvard Medical School, Boston, Massachusetts 02115, USA. | lld:pubmed |
| pubmed-article:7664346 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:7664346 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:7664346 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:7664346 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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