| pubmed-article:8051093 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C0035647 | lld:lifeskim |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C0149784 | lld:lifeskim |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C0007595 | lld:lifeskim |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C0079904 | lld:lifeskim |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C0079419 | lld:lifeskim |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C1879547 | lld:lifeskim |
| pubmed-article:8051093 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
| pubmed-article:8051093 | pubmed:issue | 31 | lld:pubmed |
| pubmed-article:8051093 | pubmed:dateCreated | 1994-9-8 | lld:pubmed |
| pubmed-article:8051093 | pubmed:abstractText | The tumor suppressor p53 is a potent transcriptional activator that has been shown to regulate its own expression. In earlier studies, deletion analysis and site-specific mutagenesis identified the p53-responsive element that fits the p53 consensus sequence. In addition, the p53-responsive element was predicted to be a binding site for NF-kappa B. In this study, we showed that NF-kappa B present in HeLa nuclear extracts could bind the same DNA element in a sequence-specific manner. Co-transfection experiments showed that the p65 subunit of NF-kappa B, but not the p50 subunit, could activate the p53 promoter. In HeLa cells, tumor necrosis factor alpha (TNF-alpha) induced NF-kappa B activity. The p53 promoter was also induced by TNF-alpha under the same conditions. Both p65 transactivation and TNF-alpha induction of the p53 promoter depended on an intact NF-kappa B site. Detailed mutational analysis of the p53 and NF-kappa B responsive elements allowed differentiation of these two responses. Thus, we show that NF-kappa B activates p53 and that this activation is inducible by TNF-alpha. Since NF-kappa B induction occurs as a response to stress and p53 arrests cells in G1/S, where repair may be initiated, activation of p53 by NF-kappa B could be a mechanism by which cells can recover from stress. | lld:pubmed |
| pubmed-article:8051093 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8051093 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8051093 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:8051093 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:8051093 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8051093 | pubmed:month | Aug | lld:pubmed |
| pubmed-article:8051093 | pubmed:issn | 0021-9258 | lld:pubmed |
| pubmed-article:8051093 | pubmed:author | pubmed-author:WuHH | lld:pubmed |
| pubmed-article:8051093 | pubmed:author | pubmed-author:LozanoGG | lld:pubmed |
| pubmed-article:8051093 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8051093 | pubmed:day | 5 | lld:pubmed |
| pubmed-article:8051093 | pubmed:volume | 269 | lld:pubmed |
| pubmed-article:8051093 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8051093 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8051093 | pubmed:pagination | 20067-74 | lld:pubmed |
| pubmed-article:8051093 | pubmed:dateRevised | 2008-11-21 | lld:pubmed |
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| pubmed-article:8051093 | pubmed:year | 1994 | lld:pubmed |
| pubmed-article:8051093 | pubmed:articleTitle | NF-kappa B activation of p53. A potential mechanism for suppressing cell growth in response to stress. | lld:pubmed |
| pubmed-article:8051093 | pubmed:affiliation | Department of Molecular Genetics, University of Texas M. D. Anderson Cancer Center, Houston 77030. | lld:pubmed |
| pubmed-article:8051093 | pubmed:publicationType | Journal Article | lld:pubmed |
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