pubmed-article:16832342 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0022567 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0108685 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0038952 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0678226 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0441889 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0205216 | lld:lifeskim |
pubmed-article:16832342 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:16832342 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:16832342 | pubmed:dateCreated | 2007-1-19 | lld:pubmed |
pubmed-article:16832342 | pubmed:abstractText | Recent studies have identified roles for C/EBPbeta in cellular survival and tumorigenesis, however, the mechanisms through which C/EBPbeta regulates these processes are not fully understood. Previously, we demonstrated that C/EBPbeta(-/-) mice are resistant to carcinogen-induced skin tumorigenesis and in response to topical carcinogen treatment display a 17-fold increase in keratinocyte apoptosis compared to wild-type mice. Here, we have investigated the mechanisms through which C/EBPbeta regulates apoptosis in response to carcinogenic stress. Analysis of carcinogen-treated C/EBPbeta(-/-) mouse skin revealed a striking increase in the number of p53 immunopositive keratinocytes in the epidermis of C/EBPbeta(-/-) mice compared to wild-type mice and this increase was temporally associated with a concomitant anomalous increase in apoptosis. The increased levels of p53 were functional as Mdm2, Bcl-2, C/EBPalpha and p21 were differentially regulated in the epidermis of carcinogen-treated C/EBPbeta(-/-) mice. The increase in p53 protein was not associated with an increase in p53 mRNA levels. To determine whether p53 is required for the increased apoptosis in C/EBPbeta(-/-) mice, C/EBPbeta/p53 compound knockout mice were generated. Carcinogen-treated C/EBPbeta/p53 compound knockout mice did not display increased apoptosis demonstrating p53 is required for the proapoptotic phenotype in C/EBPbeta(-/-) mice. Our results demonstrate that altered keratinocyte survival in C/EBPbeta(-/-) mice results from aberrant regulation of p53 protein and function and indicate C/EBPbeta has a role in the negative regulation of p53 protein levels in response to carcinogen-induced stress. | lld:pubmed |
pubmed-article:16832342 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:language | eng | lld:pubmed |
pubmed-article:16832342 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:16832342 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16832342 | pubmed:month | Jan | lld:pubmed |
pubmed-article:16832342 | pubmed:issn | 0950-9232 | lld:pubmed |
pubmed-article:16832342 | pubmed:author | pubmed-author:SmartR CRC | lld:pubmed |
pubmed-article:16832342 | pubmed:author | pubmed-author:YoonKK | lld:pubmed |
pubmed-article:16832342 | pubmed:author | pubmed-author:ZinKK | lld:pubmed |
pubmed-article:16832342 | pubmed:author | pubmed-author:EwingS JSJ | lld:pubmed |
pubmed-article:16832342 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16832342 | pubmed:day | 18 | lld:pubmed |
pubmed-article:16832342 | pubmed:volume | 26 | lld:pubmed |
pubmed-article:16832342 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16832342 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16832342 | pubmed:pagination | 360-7 | lld:pubmed |
pubmed-article:16832342 | pubmed:dateRevised | 2007-12-3 | lld:pubmed |
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pubmed-article:16832342 | pubmed:year | 2007 | lld:pubmed |
pubmed-article:16832342 | pubmed:articleTitle | Decreased survival of C/EBP beta-deficient keratinocytes is due to aberrant regulation of p53 levels and function. | lld:pubmed |
pubmed-article:16832342 | pubmed:affiliation | Cell Signaling and Cancer Group, Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695-7633, USA. | lld:pubmed |
pubmed-article:16832342 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16832342 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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