|  Help  |  About  |  Contact Us

Publication : Cell type- and differentiation-dependent expression from the mouse acetylcholine receptor epsilon-subunit promoter.

First Author  Sunyer T Year  1993
Journal  J Neurosci Res Volume  36
Issue  2 Pages  224-34
PubMed ID  8263973 Mgi Jnum  J:14842
Mgi Id  MGI:63002 Doi  10.1002/jnr.490360213
Citation  Sunyer T, et al. (1993) Cell type- and differentiation-dependent expression from the mouse acetylcholine receptor epsilon-subunit promoter. J Neurosci Res 36(2):224-34
abstractText  The nicotinic acetylcholine receptor (AChR) in adult skeletal muscle is composed of alpha-, beta-, epsilon-, and delta-subunits and is localized at the neuromuscular junction; in contrast, the more diffusely distributed fetal form is composed of alpha-, beta-, gamma-, and delta-subunits. To define sequences necessary for the transcriptional regulation of the mouse epsilon-subunit gene, we sequenced and analyzed 1036 bp upstream of the transcription start site. Using deletion analysis of the 5'-flanking region linked to the bacterial chloramphenicol acetyltransferase (CAT) gene and transfection of the resulting constructs into established cell lines, we demonstrate that a 151 bp fragment exhibits cell type- and differentiation-specific promoter activity. This activity was independent of a myogenic factor putative binding site (E-box). However, transactivation experiments with recombinant myoD, myogenin, or MRF4 showed that the E-box was functional and that MRF4 preferentially transactivates the epsilon-promoter. Thus, like other AChR promoters, the proximal region of the epsilon-promoter contains information for cell type-specific and developmental regulation of CAT and can be transactivated by myogenic factors in cultured cell lines. Unlike the other AChR promoters characterized to date, epsilon-promoter function can be partially independent of myogenic factors of the helix-loop-helix class.
Quick Links:
 
Quick Links:
 

Expression

Publication --> Expression annotations

 

Other

2 Authors

1 Bio Entities

0 Expression