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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
2001-2-22
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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.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-10022864,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-10508588,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-10679283,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-1710770,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-2030941,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-2116003,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-2138707,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-2440339,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-2466559,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-3601678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-4705382,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-6090941,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-7539118,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-7559652,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-7737130,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-7784077,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-7923365,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8137421,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8325898,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8413289,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8444876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8650547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8703044,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8895468,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8910550,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8918868,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-8978682,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-9205083,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-9305758,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-9388198,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11160903-942051
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1362-4962
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
1
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pubmed:volume |
29
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
792-8
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:11160903-3T3 Cells,
pubmed-meshheading:11160903-Animals,
pubmed-meshheading:11160903-Base Sequence,
pubmed-meshheading:11160903-Binding Sites,
pubmed-meshheading:11160903-CCAAT-Binding Factor,
pubmed-meshheading:11160903-CCAAT-Enhancer-Binding Proteins,
pubmed-meshheading:11160903-DNA,
pubmed-meshheading:11160903-Mice,
pubmed-meshheading:11160903-Molecular Sequence Data,
pubmed-meshheading:11160903-Mutation,
pubmed-meshheading:11160903-Oligonucleotides,
pubmed-meshheading:11160903-Promoter Regions, Genetic,
pubmed-meshheading:11160903-Protein Binding,
pubmed-meshheading:11160903-RNA, Messenger,
pubmed-meshheading:11160903-Response Elements,
pubmed-meshheading:11160903-Transcription Factors,
pubmed-meshheading:11160903-Transcriptional Activation,
pubmed-meshheading:11160903-Ultraviolet Rays,
pubmed-meshheading:11160903-rhoB GTP-Binding Protein
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pubmed:year |
2001
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pubmed:articleTitle |
Transcriptional activation of the small GTPase gene rhoB by genotoxic stress is regulated via a CCAAT element.
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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
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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