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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
34
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pubmed:dateCreated |
1996-10-11
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pubmed:abstractText |
Tax protein of the human T-cell lymphotropic virus type 1 (HTLV-I) is critical for viral replication and is a potent transcriptional activator of viral and cellular polymerase II (pol II) genes. We report here that Tax is able to transactivate a classical pol III promoter, VA-I. In cotransfection experiments, Tax is shown to increase transcription of the VA-I promoter approximately 25-fold. Moreover, Tax is able to activate VA-I transcription when added exogenously to an in vitro transcription reaction. Using Tax affinity column chromatography, we demonstrate that Tax is able to deplete a HeLa cell extract for components required for transcription of VA-I. The transcriptional activity of the Tax-depleted extract can be restored by the 0.6 phosphocellulose fraction. Interestingly, a consensus binding site for cAMP-responsive element binding protein (CREB) is located upstream of the VA-I promoter, and deletion of this element results in the loss of Tax responsiveness. When this CREB binding site is replaced by a Gal-4 binding site, the VA-I promoter can be transactivated by a Gal4-Tax fusion protein. Taken together, these results suggest that Tax may activate pol III and pol II promoter through a similar mechanism involving the CREB activation pathway. It is also possible that Tax affects pol III transcription by direct interaction with a component of the pol III transcriptional machinery.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cyclic AMP Response...,
http://linkedlifedata.com/resource/pubmed/chemical/DNA Primers,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Gene Products, tax,
http://linkedlifedata.com/resource/pubmed/chemical/RNA Polymerase III
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0021-9258
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
23
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pubmed:volume |
271
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
20501-6
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8702791-Base Sequence,
pubmed-meshheading:8702791-Binding Sites,
pubmed-meshheading:8702791-Consensus Sequence,
pubmed-meshheading:8702791-Cyclic AMP Response Element-Binding Protein,
pubmed-meshheading:8702791-DNA Primers,
pubmed-meshheading:8702791-DNA-Binding Proteins,
pubmed-meshheading:8702791-Gene Expression Regulation, Viral,
pubmed-meshheading:8702791-Gene Products, tax,
pubmed-meshheading:8702791-HeLa Cells,
pubmed-meshheading:8702791-Human T-lymphotropic virus 1,
pubmed-meshheading:8702791-Humans,
pubmed-meshheading:8702791-Molecular Sequence Data,
pubmed-meshheading:8702791-Promoter Regions, Genetic,
pubmed-meshheading:8702791-RNA Polymerase III,
pubmed-meshheading:8702791-Sequence Alignment,
pubmed-meshheading:8702791-Transcriptional Activation
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pubmed:year |
1996
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pubmed:articleTitle |
Human T-cell leukemia virus type I Tax protein transactivates RNA polymerase III promoter in vitro and in vivo.
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pubmed:affiliation |
Laboratory of Molecular Virology, NCI, National Institutes of Health, Bethesda, Maryland 20892, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study
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