A Novel Complex Regulates cardiac actin Gene Expression through Interaction of Emb, a Class VI POU Domain Protein, MEF2D, and the Histone Transacetylase p300
Molecular and Cellular Biology, ISSN: 0270-7306, Vol: 24, Issue: 7, Page: 2944-2957
2004
- 21Citations
- 36Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations21
- Citation Indexes21
- 21
- CrossRef18
- Captures36
- Readers36
- 36
Article Description
Expression of the mouse cardiac actin gene depends on a distal enhancer (-7 kbp) which has been shown, in transgenic mice, to direct expression to embryonic skeletal muscle. The presence of this distal sequence is also associated with reproducible expression of cardiac actin transgenes. In differentiated skeletal muscle cells, activity of the enhancer is driven by an E box, binding MyoD family members, and by a 3′ AT-rich sequence which is in the location of a DNase I-hypersensitive site. This sequence does not bind MEF2 proteins, or other known muscle transcription factors, directly. Oct1 and Emb, a class VI POU domain protein, bind to consensus sites on the DNA, and it is the binding of Emb which is important for activity. Emb binds as a major complex with MEF2D and the histone transacetylase p300. The form of Emb present in this complex and as a major form in muscle cell extracts is longer (80 kDa) than that previously described. These results demonstrate the importance of this novel complex in the transcriptional regulation of the cardiac actin gene and suggest a potential role in chromatin remodeling associated with muscle gene activation.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=1642335533&origin=inward; http://dx.doi.org/10.1128/mcb.24.7.2944-2957.2004; http://www.ncbi.nlm.nih.gov/pubmed/15024082; https://www.tandfonline.com/doi/full/10.1128/MCB.24.7.2944-2957.2004; http://mcb.asm.org/cgi/doi/10.1128/MCB.24.7.2944-2957.2004; https://syndication.highwire.org/content/doi/10.1128/MCB.24.7.2944-2957.2004; https://dx.doi.org/10.1128/mcb.24.7.2944-2957.2004; https://mcb.asm.org/content/24/7/2944
Informa UK Limited
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