| pubmed-article:2355919 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2355919 | lifeskim:mentions | umls-concept:C0019169 | lld:lifeskim |
| pubmed-article:2355919 | lifeskim:mentions | umls-concept:C0029246 | lld:lifeskim |
| pubmed-article:2355919 | lifeskim:mentions | umls-concept:C0205245 | lld:lifeskim |
| pubmed-article:2355919 | lifeskim:mentions | umls-concept:C0086222 | lld:lifeskim |
| pubmed-article:2355919 | lifeskim:mentions | umls-concept:C1705733 | lld:lifeskim |
| pubmed-article:2355919 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:2355919 | pubmed:dateCreated | 1990-7-20 | lld:pubmed |
| pubmed-article:2355919 | pubmed:abstractText | We have studied the functional constituents of the hepatitis B virus enhancer in a number of cell lines. The sequence of this enhancer, being embedded within an open reading frame of the virus, is in part evolutionarily frozen and therefore serves as a good model to investigate the fundamental enhancer elements. The hepatitis B virus enhancer contains three functionally important DNA sequence elements, EP, E, and NF-1a, each of which is bound by a distinct protein(s). The synergistic action of these elements accounts for all of the enhancer activity in a nonliver cell line and for most, but not all, of the activity in liver-derived cell lines. Multimers of the E but not of the EP element act as an autonomous enhancer. Conversely, a single element of either the E or the NF-1a element can act only when linked to the EP element. These results suggest that EP is a crucial enhancer element that acts only in interaction with a second enhancer element with intrinsic enhancer activity. Interestingly, a highly similar enhancer structure is found in a number of distinct viruses. | lld:pubmed |
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| pubmed-article:2355919 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2355919 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2355919 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:2355919 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2355919 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:2355919 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:2355919 | pubmed:author | pubmed-author:ShaulYY | lld:pubmed |
| pubmed-article:2355919 | pubmed:author | pubmed-author:Ben-LevyRR | lld:pubmed |
| pubmed-article:2355919 | pubmed:author | pubmed-author:FaktorOO | lld:pubmed |
| pubmed-article:2355919 | pubmed:author | pubmed-author:DiksteinRR | lld:pubmed |
| pubmed-article:2355919 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2355919 | pubmed:volume | 10 | lld:pubmed |
| pubmed-article:2355919 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2355919 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2355919 | pubmed:pagination | 3683-9 | lld:pubmed |
| pubmed-article:2355919 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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| pubmed-article:2355919 | pubmed:year | 1990 | lld:pubmed |
| pubmed-article:2355919 | pubmed:articleTitle | Functional organization of the hepatitis B virus enhancer. | lld:pubmed |
| pubmed-article:2355919 | pubmed:affiliation | Department of Molecular Genetics and Virology, Weizmann Institute of Science, Rehovot, Israel. | lld:pubmed |
| pubmed-article:2355919 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2355919 | pubmed:publicationType | Comparative Study | lld:pubmed |
| pubmed-article:2355919 | pubmed:publicationType | Research Support, U.S. Gov't, Non-P.H.S. | lld:pubmed |
| pubmed-article:2355919 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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