| First Author | Kadowaki Y | Year | 1995 |
| Journal | Proc Natl Acad Sci U S A | Volume | 92 |
| Issue | 10 | Pages | 4432-6 |
| PubMed ID | 7753823 | Mgi Jnum | J:26570 |
| Mgi Id | MGI:74014 | Doi | 10.1073/pnas.92.10.4432 |
| Citation | Kadowaki Y, et al. (1995) Dual transcriptional control by Ear3/COUP: negative regulation through the DR1 direct repeat and positive regulation through a sequence downstream of the transcriptional start site of the mouse mammary tumor virus promoter. Proc Natl Acad Sci U S A 92(10):4432-6 |
| abstractText | Ear3/COUP is an orphan member of the steroid/thyroid hormone receptor superfamily of transcription factors and binds most tightly to a direct repeat of AGGTCA with 1 nucleotide in between (DR1). Ear3/COUP also binds with a similar affinity to the palindromic thyroid hormone response element (TRE). This binding preference of Ear3/COUP is same as that of the retinoid X receptor (RXR), which is another member of the superfamily. In the present study, we identified a sequence responsible for Ear3/COUP-mediated transactivation in the region downstream of the transcription start site of the mouse mammary tumor virus promoter. This cis-acting sequence was unresponsive to RXR. When the DR1 or TRE sequence was added upstream of the promoter, transactivation by Ear3/COUP was completely abolished, whereas RXR enhanced transcription from the promoter. The mode of action of Ear3/COUP could be utilized to control complex gene expressions in morphogenesis, homeostasis, and development. |
