| pubmed-article:1532229 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C0026845 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C0027061 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C1425192 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C1521761 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C0376315 | lld:lifeskim |
| pubmed-article:1532229 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:1532229 | pubmed:issue | 4 | lld:pubmed |
| pubmed-article:1532229 | pubmed:dateCreated | 1992-4-22 | lld:pubmed |
| pubmed-article:1532229 | pubmed:abstractText | Recent studies have identified a conserved 28-bp element (HF-1) within the rat cardiac MLC-2 gene which confers cardiac muscle-specific and inducible expression during myocardial cell hypertrophy. Utilizing a combination of independent experimental approaches, this study characterizes two cardiac nuclear factors which bind to HF-1, a ubiquitous factor (HF-1a), and an A + T-rich binding factor (HF-1b) which is preferentially expressed in differentiated cardiac and skeletal muscle cells. The HF-1a binding site is located in a core region of the 28-bp conserved element, immediately upstream from the A + T-rich HF-1b site, which is homologous to the MEF-2 site found in a number of muscle genes. By a number of separate criteria (gel mobility shift, competition, and mutagenesis studies), HF-1b and MEF-2 appear to be indistinguishable and thus are either identical or closely related muscle factors. Transient assays of luciferase reporter genes containing point mutations throughout the 28-bp HF-1 regulatory element document the importance of both the HF-1a and HF-1b sites in transient assays in ventricular muscle cells. In the native 250-bp MLC-2 promoter fragment, mutations in the single E box had little effect on cardiac muscle specificity, while point mutations in either the HF-1a or HF-1b binding site significantly reduced promoter activity, underscoring the importance of both the HF-1a and HF-1b sites in the transcriptional activation of this cardiac muscle gene. Thus, this study provides evidence that a novel, ubiquitous factor (HF-1a) and a muscle factor (HF-1b/MEF-2) can form a novel, E-box-independent pathway for muscle-specific expression in ventricular cardiac muscle cells. | lld:pubmed |
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| pubmed-article:1532229 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1532229 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1532229 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1532229 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:1532229 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1532229 | pubmed:month | Apr | lld:pubmed |
| pubmed-article:1532229 | pubmed:issn | 0270-7306 | lld:pubmed |
| pubmed-article:1532229 | pubmed:author | pubmed-author:EvansS MSM | lld:pubmed |
| pubmed-article:1532229 | pubmed:author | pubmed-author:ChienK RKR | lld:pubmed |
| pubmed-article:1532229 | pubmed:author | pubmed-author:ZhuHH | lld:pubmed |
| pubmed-article:1532229 | pubmed:author | pubmed-author:GarciaA VAV | lld:pubmed |
| pubmed-article:1532229 | pubmed:author | pubmed-author:Navankasattus... | lld:pubmed |
| pubmed-article:1532229 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1532229 | pubmed:volume | 12 | lld:pubmed |
| pubmed-article:1532229 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1532229 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1532229 | pubmed:pagination | 1469-79 | lld:pubmed |
| pubmed-article:1532229 | pubmed:dateRevised | 2010-9-7 | lld:pubmed |
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