| First Author | Lee CH | Year | 2000 |
| Journal | Biochem Pharmacol | Volume | 60 |
| Issue | 1 | Pages | 127-36 |
| PubMed ID | 10807954 | Mgi Jnum | J:62167 |
| Mgi Id | MGI:1858532 | Doi | 10.1016/s0006-2952(00)00311-7 |
| Citation | Lee CH, et al. (2000) Characterization of the mouse nuclear orphan receptor TR2-11 gene promoter and its potential role in retinoic acid-induced P19 apoptosis. Biochem Pharmacol 60(1):127-36 |
| abstractText | The complete mouse orphan nuclear receptor TR2-11 gene structure and its 5'-untranscribed region were characterized. This gene contains 14 exons, with the first exon encoding only the 5'-untranslated sequence. The regulatory region of this gene was characterized by using reporter assays that define the minimal promoter activity in a sequence 212 nucleotides upstream from the translation initiation site. Furthermore, it was concluded that splicing of intron 1 is required for efficient promoter activity. Reporters driven by this promoter were induced by retinoic acid (RA) in COS-1 cells supplied with exogenous retinoic acid receptor-alpha (RAR(alpha)) and retinoid receptor X-beta (RXR(beta)). Binding of RAR(alpha)/RXR(beta) to the minimal promoter region was demonstrated in gel retardation assays. In P19 cells, both the endogenous TR2-11 gene and the reporters driven by this promoter were induced by RA in a protein synthesis-independent manner, and overexpression of TR2-11 protein resulted in cellular apoptosis in the absence of RA. The regulation of TR2-11 by RA and the implication of TR2 up-regulation in P19 cellular apoptosis are discussed. |
