Human TAF(parallel to)28 promotes transcriptional stimulation by activation function 2 of the retinoid X receptors

被引:75
作者
May, M [1 ]
Mengus, G [1 ]
Lavigne, AC [1 ]
Chambon, P [1 ]
Davidson, I [1 ]
机构
[1] ULP,INST GENET & BIOL MOL & CELLULAIRE,INSERM,COLL FRANCE,CNRS,F-67404 ILLKIRCH GRAFFENS,FRANCE
关键词
oestrogen receptor; TFIID; transcriptional intermediary factors; vitamin D3 receptor;
D O I
10.1002/j.1460-2075.1996.tb00672.x
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Transcriptional activation in vitro involves direct interactions of transactivators with the TATA binding protein (TBP) and the TBP-associated factors (TAF(II)s) which constitute the TFIID complex, However, the role of TAF(II)s in transcriptional regulation in mammalian cells has not been addressed. We show that activation function 2 of the retinoid X receptors (RXR AF-2) does not activate transcription from a minimal promoter in Cos cells, However, coexpression of human (h) TAF(II)28 promotes a strong ligand-dependent activity of the RXR AF-2 on a minimal promoter and potentiates the ability of the RXR alpha AF-2 to activate transcription from a complex promoter, The expression of hTAF(II)28 also potentiated transactivation by several nuclear receptors, notably the oestrogen and vitamin D3 receptors (ER and VDR), whereas other classes of activator were not affected. The effect of hTAF(II)28 on RXR AF-2 activities did not appear to require direct RXR-TAF(II)28 interactions, but correlated with the ability of hTAF(II)28 to interact with TBP. In contrast to Cos cells, the RXR AF-2s had differential abilities to activate transcription from a minimal promoter in HeLa cells, and a lesser increase in their activity was observed upon hTAF(II)28 coexpression. Moreover, coexpression of hTAF(II)28 did not increase but rather repressed activation by the ER and VDR AF-2s in HeLa cells. In agreement with these data, showing that TAF(II)28 is limiting in the AF-2 activation pathway in Cos cells, TAF(II)28 is selectively depleted in Cos cell TFIID.
引用
收藏
页码:3093 / 3104
页数:12
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