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TR4 orphan nuclear receptor functions as an apoptosis modulator via regulation of Bcl-2 gene expression.


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 (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.

SUBMITTER: Kim E 

PROVIDER: S-EPMC2121606 | biostudies-literature | 2007 Sep

REPOSITORIES: biostudies-literature

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TR4 orphan nuclear receptor functions as an apoptosis modulator via regulation of Bcl-2 gene expression.

Kim Eungseok E   Ma Wen-Lung WL   Lin Din-Lii DL   Inui Shigeki S   Chen Yuh-Ling YL   Chang Chawnshang C  

Biochemical and biophysical research communications 20070710 2


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 casp  ...[more]

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