pubmed-article:2111440 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0678108 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0021027 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0232920 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0040649 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0086860 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C0086222 | lld:lifeskim |
pubmed-article:2111440 | lifeskim:mentions | umls-concept:C1705733 | lld:lifeskim |
pubmed-article:2111440 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:2111440 | pubmed:dateCreated | 1990-6-25 | lld:pubmed |
pubmed-article:2111440 | pubmed:abstractText | We demonstrate that the immunoglobulin heavy-chain enhancer functions as the promoter for I mu sterile transcription. The enhancer itself, when placed 5' to the bacterial cat or neo genes, is able to direct transcription by using heterogeneous start sites that are generally the same as those found with bona fide I mu transcripts. In general, promoter activity is dependent on the same sequence motifs important for enhancer activity. However, it appears that a mutation within the conserved octanucleotide ATTTGCAT has a much more severe effect on the promoter activity of the enhancer than the same mutation has on its enhancer activity. This result is consistent with the known role of the octanucleotide as a promoter element, and this is discussed in relation to the biological role of sterile transcription. | lld:pubmed |
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pubmed-article:2111440 | pubmed:language | eng | lld:pubmed |
pubmed-article:2111440 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:2111440 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:2111440 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:2111440 | pubmed:month | Jun | lld:pubmed |
pubmed-article:2111440 | pubmed:issn | 0270-7306 | lld:pubmed |
pubmed-article:2111440 | pubmed:author | pubmed-author:ToL BLB | lld:pubmed |
pubmed-article:2111440 | pubmed:author | pubmed-author:KadeschTT | lld:pubmed |
pubmed-article:2111440 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:2111440 | pubmed:volume | 10 | lld:pubmed |
pubmed-article:2111440 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:2111440 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:2111440 | pubmed:pagination | 2619-24 | lld:pubmed |
pubmed-article:2111440 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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pubmed-article:2111440 | pubmed:year | 1990 | lld:pubmed |
pubmed-article:2111440 | pubmed:articleTitle | The immunoglobulin heavy-chain enhancer functions as the promoter for I mu sterile transcription. | lld:pubmed |
pubmed-article:2111440 | pubmed:affiliation | Howard Hughes Medical Institute, University of Pennsylvania School of Medicine, Philadelphia 19104-6072. | lld:pubmed |
pubmed-article:2111440 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:2111440 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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