| First Author | Kim E | Year | 2007 |
| Journal | Biochem Biophys Res Commun | Volume | 361 |
| Issue | 2 | Pages | 323-8 |
| PubMed ID | 17655826 | Mgi Jnum | J:123473 |
| Mgi Id | MGI:3718717 | Doi | 10.1016/j.bbrc.2007.06.168 |
| Citation | Kim E, et al. (2007) TR4 orphan nuclear receptor functions as an apoptosis modulator via regulation of Bcl-2 gene expression. Biochem Biophys Res Commun 361(2):323-328 |
| abstractText | While Bcl-2 plays an important role in cell apoptosis, its relationship to the orphan nuclear receptors remains unclear. Here we report that mouse embryonic fibroblast (MEF) cells prepared from TR4-deficient (TR4(-)(/-)) mice are more susceptible to UV-irradiation mediated apoptosis compared to TR4-Wildtype (TR4(+/+)) littermates. Substantial increasing TR4(-)(/-) MEF apoptosis to UV-irradiation was correlated to the down-regulation of Bcl-2 RNA and protein expression and collaterally increased caspase-3 activity. Furthermore, this TR4-induced Bcl-2 gene expression can be suppressed by co-transfection with TR4 coregulators, such as androgen receptor (AR) and receptor-interacting protein 140 (RIP140) in a dose-dependent manner. Together, our results demonstrate that TR4 might function as an apoptosis modulator through induction of Bcl-2 gene expression. |
