| Literature DB >> 8147894 |
J G Edwards1, J J Bahl, I L Flink, S Y Cheng, E Morkin.
Abstract
3,5,3'-Triiodo-L-thyronine (T3) regulation of beta-MHC expression was studied in rat fetal heart cells using deletion mutants of both the rat and human promoter regions fused to a CAT expression vector. T3 inhibited the expression of human and rat beta-MHC constructs with an IC50 of about 1nM, which was similar to the EC50 for beta MHC-mRNA observed in cardiomyocytes. Deletion analysis of beta MHC promoter constructs suggested that a T3 response element (TRE) is located near the start of transcription. Possibly, T3-receptor binding at this site interferes with formation of the transcriptional initiation complex.Entities:
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Year: 1994 PMID: 8147894 DOI: 10.1006/bbrc.1994.1398
Source DB: PubMed Journal: Biochem Biophys Res Commun ISSN: 0006-291X Impact factor: 3.575