The orphan nuclear receptor DAX-1 acts as a novel transcriptional corepressor of PPARγ
- 作者：Gwang Sik Kim ; Gha Young Lee ; Balach ; ar Nedumaran ; Yun-Yong Park ; Kyung Tae Kim ; Sang Chul Park ; Young Chul Lee ; Jae Bum Kim ; Hueng-Sik Choi
- 关键词：Orphan nuclear receptor ; DAX-1 ; PPARγ ; Corepressor ; PGC-1
//www.sciencedirect.com/scidirimg/entities/204e.gif" alt="greek small letter alpha" title="greek small letter alpha" border="0"> ; Adipogenesis
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：2008
- 期刊代码：159_0006291x
- 类别：bio
- 出版时间：30 May 2008
- 卷：370
- 期：2
- 页码：264-268
- 文件大小：552 K
摘要
DAX-1 is an atypical nuclear receptor (NR) which functions primarily as a transcriptional corepressor of other NRs via heterodimerization. Peroxisome proliferator-activated receptor (PPAR) γ is a ligand-dependent NR which performs a key function in adipogenesis. In this study, we evaluated a novel cross-talk mechanism between DAX-1 and PPARγ. Transient transfection assays demonstrated that DAX-1 inhibits the transactivity of PPARγ in a dose-dependent manner. DAX-1 directly competed with the PPARγ coactivator (PGC)-1
for binding to PPARγ. Endogenous levels of DAX-1 were significantly lower in differentiated 3T3-L1 adipocytes as compared to preadipocytes. Using a retroviral expression system, we demonstrated that DAX-1 overexpression downregulates the expression of PPARγ target genes, resulting in an attenuation of adipogenesis in 3T3-L1 cells. Our results suggest that DAX-1 acts as a corepressor of PPARγ and performs a potential function in the regulation of PPARγ-mediated cellular differentiation.
for binding to PPARγ. Endogenous levels of DAX-1 were significantly lower in differentiated 3T3-L1 adipocytes as compared to preadipocytes. Using a retroviral expression system, we demonstrated that DAX-1 overexpression downregulates the expression of PPARγ target genes, resulting in an attenuation of adipogenesis in 3T3-L1 cells. Our results suggest that DAX-1 acts as a corepressor of PPARγ and performs a potential function in the regulation of PPARγ-mediated cellular differentiation.