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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
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pubmed:dateCreated |
1994-8-15
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pubmed:abstractText |
The transcriptional down-regulation of the major histocompatibility complex (MHC) class I antigens in adenovirus type 12 (Ad12) transformed cells gives them the potential to escape immunosurveillance and to form tumors. The enhancer of the class I promoter is the target of transcriptional repression which is mediated by the E1A gene of Ad12. The R2 region within the class I enhancer acts as a negative element in Ad12-transformed cells and exhibits a stronger binding activity than is observed in nontumorigenic Ad5-transformed cells, which are not reduced in class I expression. The R2 element contains a nuclear hormone receptor half-site consensus sequence, AGGTCA, which is required for both the binding activity and the ability of R2 to act as a negative element in Ad12-transformed cells. In this study, we show that an orphan hormone receptor protein, COUP-TF, contributes to the differential R2 binding activity observed between Ad12- and Ad5-transformed cells. Additionally, COUP-TF was shown to bind as a dimer to the R2 element and to use the consensus AGGTCA as one half-site and its 3' flanking sequence as a probable second degenerate half-site. Since COUP-TF can act as a transcriptional repressor, we suggest that the higher COUP-TF binding activity to the R2 element in Ad12-transformed cells contributes to down-regulation of class I transcription and, consequently, tumorigenesis.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/COUP Transcription Factor I,
http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/NR2F1 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/Nr2f1 protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/Recombinant Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
0950-9232
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2183-90
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:8036004-Adenoviruses, Human,
pubmed-meshheading:8036004-Animals,
pubmed-meshheading:8036004-Base Sequence,
pubmed-meshheading:8036004-COUP Transcription Factor I,
pubmed-meshheading:8036004-Cell Transformation, Neoplastic,
pubmed-meshheading:8036004-DNA-Binding Proteins,
pubmed-meshheading:8036004-Down-Regulation,
pubmed-meshheading:8036004-Enhancer Elements, Genetic,
pubmed-meshheading:8036004-Genes, MHC Class I,
pubmed-meshheading:8036004-Humans,
pubmed-meshheading:8036004-Mice,
pubmed-meshheading:8036004-Mice, Inbred BALB C,
pubmed-meshheading:8036004-Molecular Sequence Data,
pubmed-meshheading:8036004-Recombinant Proteins,
pubmed-meshheading:8036004-Transcription Factors
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pubmed:year |
1994
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pubmed:articleTitle |
Negative regulation by the R2 element of the MHC class I enhancer in adenovirus-12 transformed cells correlates with high levels of COUP-TF binding.
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pubmed:affiliation |
Department of Microbiology, School of Dental Medicine, University of Pennsylvania, Philadelphia 19104.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
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