Abstract
Recent advances in the field of in vitro chromatin assembly have led to in vitro transcription systems which reproduce in the test tube, in vivo characteristics of ligand-dependent transcriptional activation by nuclear receptors. Dissection of these systems has begun to provide us with information concerning the underlying molecular mechanisms. Through recruitment of coactivator proteins, nuclear receptors act first to remodel chromatin within the promoter region and then to recruit the transcriptional machinery to the promoter region in order to initiate transcription. Here we present a possible sequential mechanism for ligand-dependent transcriptional activation by nuclear receptors and discuss the in vitro and in vivo data that support this model.
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Abbreviations
- AF-1:
-
ligand-independent activation function
- AF-2:
-
ligand-dependent activation function
- ChIP:
-
chromatin immunoprecipitation
- DBD:
-
DNA binding domain
- ER:
-
estrogen receptor
- GR:
-
glucocorticoid receptor
- LBD:
-
ligand binding domain
- NR:
-
nuclear receptor
- PolII:
-
RNA polymerase II
- PPAR:
-
peroxisome proliferator-activator receptor
- PR:
-
progesterone receptor
- RA:
-
retinoic acid
- RAR:
-
retinoic acid receptor
- RE:
-
response element
- RXR:
-
retinoid X receptor
- SF1:
-
steroidogenic factor 1
- TR:
-
thyroid hormone receptor
- VDR:
-
vitamin D receptor.
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Acknowledgements
We thank Marjorie Brand, Catherine Fromental-Ramain, Laurent Gelman and Frank Vreede for useful discussions and for critically reading the manuscript. Work performed at the IGBMC was supported by grants from the Centre National de la Recherche Scientifique, the Institut National de la Santé et de la Recherche Médicale, the Collège de France, the Centre Hospitalier Universitaire Régional, the Association pour la Recherche sur la Cancer, the Fondation pour la Recherche Médicale and Bristol-Myers Squibb.
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Dilworth, F., Chambon, P. Nuclear receptors coordinate the activities of chromatin remodeling complexes and coactivators to facilitate initiation of transcription. Oncogene 20, 3047–3054 (2001). https://doi.org/10.1038/sj.onc.1204329
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