- 作者: J. Du; C. Nan; J. J. Huang; C. Zhang; J. Liu; P. Jia; M. Abers; X. P. Huang
- 作者服務機構: Department of Biomedical Science, Center for MolecularBiology and Biotechnology, USA
- 中文摘要: --
- 英文摘要: Two major troponin I (TnI) genes, fetal TnI(ssTnI) and adult TnI (cTnI), are expressed in the mammalianheart under the control of a developmentallyregulated program. In this study, the up-stream domain(*1,800 bp) of mouse fetal TnI gene has been cloned andcharacterized. There is a high homology of this regionamong mouse, rat and human. Analysis of the sequencerevealed several putative regulatory domains and bindingsites (Sp1 binding sites, GATA binding site, MyoD, CREB,MEF2, AP1, NFjB, etc). Transfection assays indicated thatconserved GA-rich sequences, CREB and a CCAAT boxwithin the first 300 bp upstream of the transcription startsite were critical for the gene expression. Electrophoreticmobility shift assays (EMSAs) and chromatin immunoprecipitation(ChIP) assays revealed binding proteins to CREBsite in nuclear extracts from myocardial cells. An inhibitorydomain was revealed within the sequence between -1,700to -1,780. Thyroid hormone (T3) caused a significantinhibitory effect on ssTnI expression in myocardial cellswhereas this effect was not evident in CHO cells.
- 中文關鍵字: --
- 英文關鍵字: Myofibril protein; Slow skeletal troponin I; Gene regulation; Thyroid hormone; Myocardium