Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
10767037 | Biochemical and Biophysical Research Communications | 2007 | 6 Pages |
Abstract
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 (TR4â/â) mice are more susceptible to UV-irradiation mediated apoptosis compared to TR4-Wildtype (TR4+/+) littermates. Substantial increasing TR4â/â 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.
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Authors
Eungseok Kim, Wen-Lung Ma, Din-Lii Lin, Shigeki Inui, Yuh-Ling Chen, Chawnshang Chang,