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Nuclear receptors coordinate the activities of chromatin remodeling complexes and coactivators to facilitate initiation of transcription
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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“In the absence of ligand, transcription is turned “off” by RXR/RAR heterodimers bound to DNA and associated to corepressor complexes”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [89]
In the citing paper
“According to the current model of gene regulation by RARs ( 89 ), in the absence of ligand, the DNA-bound RAR ␣ subtype is associated with corepressors, which serve as adaptors recruiting high molecular weight complexes endowed with histone deacetylase (HDAC) activity ( 90 ).”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [89]
In the citing paper
“These complexes deacetylate lysine residues in the N-terminal tails of histones and maintain chromatin in a condensed, repressed state over the target promoter ( 35, 89 ) ( Fig. 4A ).”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [89]
In the citing paper
“Then, activated RARs recruit the transcription machinery, including the multisubunit Mediator complex, RNA polymerase II, and the general transcription factors ( 35, 89 ) ( Fig. 4B ).”
From Vitamin A and retinoid signaling: genomic and nongenomic effects (2013) · cites this paper as [89]
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Metadata
- Authors
- Dilworth, F. J., & Chambon, P.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- Venue
- Oncogene
- Published
- 2001-05-28
- Volume
- 20
- Issue
- 24
- Pages
- 3047-3054
- ISSN
- 0950-9232 (ISSN-L)
- 1476-5594
- OpenAlex
- W2315037039
- Cited by
- 269
- References
- 83
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 6 · 2023: 3 · 2022: 6 · 2021: 2 · 2020: 3 · 2019: 8 · 2018: 6 · 2017: 7 · 2016: 10 · 2015: 13 · 2014: 9 · 2013: 9 · 2012: 10
- FWCI
- 1.58
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Oncogene (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Chromatin Remodeling and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- nuclear receptors, chromatin remodeling, transcriptional coactivator, transcription initiation, in vitro transcription system, chromatin assembly
- MeSH terms
- Animals, Chromatin, Humans, Models, Biological, Transcription, Genetic, Trans-Activators, Receptors, Cytoplasmic and Nuclear
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