| pubmed-article:12443538 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:12443538 | lifeskim:mentions | umls-concept:C0225668 | lld:lifeskim |
| pubmed-article:12443538 | lifeskim:mentions | umls-concept:C0332197 | lld:lifeskim |
| pubmed-article:12443538 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
| pubmed-article:12443538 | lifeskim:mentions | umls-concept:C1155873 | lld:lifeskim |
| pubmed-article:12443538 | lifeskim:mentions | umls-concept:C1517945 | lld:lifeskim |
| pubmed-article:12443538 | pubmed:dateCreated | 2003-2-6 | lld:pubmed |
| pubmed-article:12443538 | pubmed:abstractText | The p53 oncosuppressor protein is a critical mediator of the response to injury in mammalian cells and is mutationally inactivated in the majority of lung malignancies. In this analysis, the effects of p53-deficiency were investigated in short-term primary cultures of murine bronchiolar Clara cells. Clara cells, isolated from gene-targeted p53-deficient mice, were compared to cells derived from wild type littermates. | lld:pubmed |
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| pubmed-article:12443538 | pubmed:language | eng | lld:pubmed |
| pubmed-article:12443538 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:12443538 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:12443538 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:12443538 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:12443538 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:12443538 | pubmed:issn | 1471-2121 | lld:pubmed |
| pubmed-article:12443538 | pubmed:author | pubmed-author:ClarkeAlan... | lld:pubmed |
| pubmed-article:12443538 | pubmed:author | pubmed-author:HarrisonDavid... | lld:pubmed |
| pubmed-article:12443538 | pubmed:author | pubmed-author:ArmitChristop... | lld:pubmed |
| pubmed-article:12443538 | pubmed:author | pubmed-author:O'DeaShirleyS | lld:pubmed |
| pubmed-article:12443538 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:12443538 | pubmed:day | 21 | lld:pubmed |
| pubmed-article:12443538 | pubmed:volume | 3 | lld:pubmed |
| pubmed-article:12443538 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:12443538 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:12443538 | pubmed:pagination | 27 | lld:pubmed |
| pubmed-article:12443538 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:12443538 | pubmed:year | 2002 | lld:pubmed |
| pubmed-article:12443538 | pubmed:articleTitle | Absence of p53 in Clara cells favours multinucleation and loss of cell cycle arrest. | lld:pubmed |
| pubmed-article:12443538 | pubmed:affiliation | CRC Laboratories, Department of Pathology, University of Edinburgh, Teviot Place, Edinburgh EH8 9AG, UK. chrisa@hgu.mrc.ac.uk | lld:pubmed |
| pubmed-article:12443538 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:12443538 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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