pubmed-article:11160903 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:11160903 | lifeskim:mentions | umls-concept:C1257899 | lld:lifeskim |
pubmed-article:11160903 | lifeskim:mentions | umls-concept:C0751984 | lld:lifeskim |
pubmed-article:11160903 | lifeskim:mentions | umls-concept:C0162493 | lld:lifeskim |
pubmed-article:11160903 | lifeskim:mentions | umls-concept:C1333729 | lld:lifeskim |
pubmed-article:11160903 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
pubmed-article:11160903 | lifeskim:mentions | umls-concept:C0013879 | lld:lifeskim |
pubmed-article:11160903 | pubmed:issue | 3 | lld:pubmed |
pubmed-article:11160903 | pubmed:dateCreated | 2001-2-22 | lld:pubmed |
pubmed-article:11160903 | pubmed:abstractText | The gene encoding the Ras-related GTPase RhoB-specific is immediate-early inducible by genotoxic treatments. Regulation of transcriptional activation of rhoB is still unclear. Here we show that cells lacking either p53 or c-Fos are not different from wild-type cells with respect to the level of rhoB induction upon UV irradiation, indicating that these transcription factors are not crucial for stimulation of rhoB mRNA expression. Extracts from UV-irradiated and non-irradiated cells revealed similar DNA-binding activities to a 0.17 kb rhoB promoter fragment harboring the functional element(s) necessary for stimulation of rhoB by UV light. By means of immunoprecipitation we found that an ATF-2-specific antibody co-precipitates the (32)P-labeled 0.17 kb rhoB fragment, whereas an anti-AP1 antibody did not. Since no consensus sequence for binding of ATF-2 is present within the rhoB promoter, ATF-2 is likely to be associated with another factor that binds to the minimal promoter. Deletion analysis and site-directed mutagenesis of the 0.17 kb rhoB fragment revealed a CCAAT box to be an essential requirement for stimulation of rhoB by UV light and methyl methanesulfonate. Moreover, immunoprecipitation experiments showed that the CCAAT-binding factor NF-YA is complexed with ATF-2. Overall, the data strongly indicate that transcriptional activation of the rhoB gene by genotoxic stress is regulated via a CCAAT box and that interaction of CCAAT-binding factor and ATF-2 triggers the stress-inducible expression of rhoB. | lld:pubmed |
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pubmed-article:11160903 | pubmed:language | eng | lld:pubmed |
pubmed-article:11160903 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11160903 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:11160903 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:11160903 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:11160903 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:11160903 | pubmed:month | Feb | lld:pubmed |
pubmed-article:11160903 | pubmed:issn | 1362-4962 | lld:pubmed |
pubmed-article:11160903 | pubmed:author | pubmed-author:FritzGG | lld:pubmed |
pubmed-article:11160903 | pubmed:author | pubmed-author:KainaBB | lld:pubmed |
pubmed-article:11160903 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:11160903 | pubmed:day | 1 | lld:pubmed |
pubmed-article:11160903 | pubmed:volume | 29 | lld:pubmed |
pubmed-article:11160903 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:11160903 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:11160903 | pubmed:pagination | 792-8 | lld:pubmed |
pubmed-article:11160903 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:11160903 | pubmed:year | 2001 | lld:pubmed |
pubmed-article:11160903 | pubmed:articleTitle | Transcriptional activation of the small GTPase gene rhoB by genotoxic stress is regulated via a CCAAT element. | lld:pubmed |
pubmed-article:11160903 | pubmed:affiliation | Division of Applied Toxicology, Institute of Toxicology, University of Mainz, Obere Zahlbacher Strasse 67, D-55131 Mainz, Germany. fritz@mail.uni-mainz.de | lld:pubmed |
pubmed-article:11160903 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:11160903 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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