Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
14
|
| pubmed:dateCreated |
1995-5-15
|
| pubmed:abstractText |
The hepatitis B virus (HBV) and polyomavirus (Py) enhancer regions contain multiple cis-acting elements that contribute to enhancer activity. The EF-C binding site was previously shown to be an important functional component of each enhancer region. EF-C is a ubiquitous binding activity that interacts with an inverted repeat sequence in the HBV and Py enhancer regions. Although the EF-C binding site is required for optimal enhancer function, the EF-C site does not possess intrinsic enhancer activity when assayed in the absence of flanking elements. With both the HBV and Py enhancer regions, EF-C stimulates the activity of adjacent enhancer elements in a synergistic manner. EF-C corresponds to RFX-1, a protein that binds to a conserved and functionally important site in major histocompatibility complex (MHC) class II antigen promoter regions. Interestingly, the RFX-1 binding site in MHC class II promoters only contains an EF-C half-site, maintaining one arm of the inverted repeat in an EF-C binding site. We have investigated the binding of purified EF-C and RFX-1 to sites in the Py and HBV enhancer regions that carry mutations that either disrupt one arm of the EF-C inverted repeat, or alter the spacing between the repeats. Our results show that the interaction of EF-C and RFX-1 with an intact inverted repeat is required for functional activity of these viral enhancer regions. Chemical footprinting and modification interference assays show that the interaction of EF-C and RFX-1 with the DRA MHC class II promoter truly represents half-site interaction, and that this binding is unstable. In contrast, the binding of EF-C and RFX-1 to the viral inverted repeats is stable. These results suggest that an additional activity may be required to stabilize EF-C/RFX-1 interaction with the MHC class II promoter, and that viral enhancer regions have evolved high affinity binding sites to sequester dimeric EF-C/RFX-1.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Apr
|
| pubmed:issn |
0021-9258
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
7
|
| pubmed:volume |
270
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
8353-60
|
| pubmed:dateRevised |
2008-11-21
|
| pubmed:meshHeading |
pubmed-meshheading:7713944-3T3 Cells,
pubmed-meshheading:7713944-Animals,
pubmed-meshheading:7713944-Base Sequence,
pubmed-meshheading:7713944-Binding Sites,
pubmed-meshheading:7713944-DNA, Viral,
pubmed-meshheading:7713944-DNA-Binding Proteins,
pubmed-meshheading:7713944-Enhancer Elements, Genetic,
pubmed-meshheading:7713944-Genes, MHC Class II,
pubmed-meshheading:7713944-HeLa Cells,
pubmed-meshheading:7713944-Hepatitis B virus,
pubmed-meshheading:7713944-Humans,
pubmed-meshheading:7713944-Mice,
pubmed-meshheading:7713944-Molecular Sequence Data,
pubmed-meshheading:7713944-Polyomavirus,
pubmed-meshheading:7713944-Promoter Regions, Genetic,
pubmed-meshheading:7713944-Repetitive Sequences, Nucleic Acid,
pubmed-meshheading:7713944-Transcription Factors,
pubmed-meshheading:7713944-Transcriptional Activation
|
| pubmed:year |
1995
|
| pubmed:articleTitle |
Interaction of EF-C/RFX-1 with the inverted repeat of viral enhancer regions is required for transactivation.
|
| pubmed:affiliation |
Department of Molecular Genetics and Microbiology, State University of New York, Stony Brook 11794, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.
|