| pubmed-article:8668191 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:8668191 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:8668191 | lifeskim:mentions | umls-concept:C0162326 | lld:lifeskim |
| pubmed-article:8668191 | lifeskim:mentions | umls-concept:C0013879 | lld:lifeskim |
| pubmed-article:8668191 | lifeskim:mentions | umls-concept:C0037791 | lld:lifeskim |
| pubmed-article:8668191 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:8668191 | pubmed:dateCreated | 1996-8-8 | lld:pubmed |
| pubmed-article:8668191 | pubmed:abstractText | M-CAT elements mediate both muscle-specific and non-muscle-specific transcription. We used artificial promoters to dissect M-CAT elements derived from the cardiac troponin T promoter, whose regulation is highly striated muscle specific. We show that muscle-specific M-CAT-dependent expression requires two distinct components: the core heptameric M-CAT motif (5'-CATTCCT-3'), which constitutes the canonical binding site for TEF-1-related proteins, and specific sequences immediately flanking the core motif that bind an additional factor(s). These factors are found in higher-order M-CAT DNA-protein complexes with TEF-1 proteins. Non-muscle-specific promoters are produced when the sequences flanking the M-CAT motif are removed or modified to match those of non-muscle-specific promoters such as the simian virus 40 promoter. Moreover, a mutation of the 5'-flanking region of the cardiac troponin T M-CAT-1 element upregulated expression in nonmuscle cells. That mutation also disrupts a potential E box that apparently does not bind myogenic basic helix-loop-helix proteins. We propose a model in which M-CAT motifs are potentially active in many cell types but are modulated through protein binding to specific flanking sequences. In nonmuscle cells, these flanking sequences bind a factor(s) that represses M-CAT-dependent activity. In muscle cells, on the other hand, the factor(s) binding to these flanking sequences contributes to both the cell specificity and the overall transcriptional strength of M-CAT-dependent promoters. | lld:pubmed |
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| pubmed-article:8668191 | pubmed:language | eng | lld:pubmed |
| pubmed-article:8668191 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:8668191 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:8668191 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:8668191 | pubmed:month | Jul | lld:pubmed |
| pubmed-article:8668191 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:8668191 | pubmed:author | pubmed-author:OrdahlC PCP | lld:pubmed |
| pubmed-article:8668191 | pubmed:author | pubmed-author:FarranceI KIK | lld:pubmed |
| pubmed-article:8668191 | pubmed:author | pubmed-author:LarkinS BSB | lld:pubmed |
| pubmed-article:8668191 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:8668191 | pubmed:volume | 16 | lld:pubmed |
| pubmed-article:8668191 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:8668191 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:8668191 | pubmed:pagination | 3742-55 | lld:pubmed |
| pubmed-article:8668191 | pubmed:dateRevised | 2009-11-18 | lld:pubmed |
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