ArticleMolecular and cellular biology1994
Ligand-dependent occupancy of the retinoic acid receptor beta 2 promoter in vivo.
Article in Molecular and cellular biology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 64 citations in OpenAlex.
- Impaired retinoic acid (RA) signal leads to RARbeta2 epigenetic silencing and RA resistance.Molecular and cellular biology · 2005Article
- c-Jun N-terminal kinase contributes to aberrant retinoid signaling in lung cancer cells by phosphorylating and inducing proteasomal degradation of retinoic acid receptor alpha.Molecular and cellular biology · 2005Article
- Phosphorylation of histone H3 is functionally linked to retinoic acid receptor beta promoter activation.EMBO reports · 2002Article
- Chromosomal integration of retinoic acid response elements prevents cooperative transcriptional activation by retinoic acid receptor and retinoid X receptor.Molecular and cellular biology · 2002Article
- Review
- Cell-type-specific regulation of the retinoic acid receptor mediated by the orphan nuclear receptor TLX.Molecular and cellular biology · 2000Article
- A bromodomain protein, MCAP, associates with mitotic chromosomes and affects G(2)-to-M transition.Molecular and cellular biology · 2000Article
- Article
- Regulation of the juvenile hormone esterase gene by a composite core promoter.The Biochemical journal · 2000Article
- Article
- Retinoids: present role and future potential.British journal of cancer · 1999Review
- Retinoid-induced chromatin structure alterations in the retinoic acid receptor beta2 promoter.Molecular and cellular biology · 1997Article
- A histone deacetylase inhibitor potentiates retinoid receptor action in embryonal carcinoma cells.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Modulation of retinoic acid sensitivity in lung cancer cells through dynamic balance of orphan receptors nur77 and COUP-TF and their heterodimerization.The EMBO journal · 1997Article
- Retinoid X receptor:vitamin D3 receptor heterodimers promote stable preinitiation complex formation and direct 1,25-dihydroxyvitamin D3-dependent cell-free transcription.Molecular and cellular biology · 1997Article
- Interferon regulatory factors and TFIIB cooperatively regulate interferon-responsive promoter activity in vivo and in vitro.Molecular and cellular biology · 1996Article
- In vivo genomic footprinting of thyroid hormone-responsive genes in pituitary tumor cell lines.Molecular and cellular biology · 1996Article
- Regulation of the chicken ovalbumin gene by estrogen and corticosterone requires a novel DNA element that binds a labile protein, Chirp-1.Molecular and cellular biology · 1996Article
- Distinct stages in adipogenesis revealed by retinoid inhibition of differentiation after induction of PPARgamma.Molecular and cellular biology · 1996Article
- Retinoic acid-mediated down-regulation of Oct3/4 coincides with the loss of promoter occupancy in vivo.The EMBO journal · 1996Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoic acid (RA) activates transcription of the RA receptor beta 2 (RAR beta 2) gene in embryonal carcinoma (EC) cells. This activation involves binding of the RAR/retinoid X receptor (RAR/RXR) heterodimer to the RA-responsive element (beta RARE). Dimethyl sulfate-based genomic footprinting was performed to examine occupancy of this promoter in P19 EC cells. No footprint was detected at the beta RARE prior to RA treatment, but a footprint was detected within the first hour of RA treatment. Concomitantly, other elements in the promoter, the cyclic AMP-responsive element and tetradecanoyl phorbol acetate-like-responsive element became footprinted. Footprints at these elements were induced by RA without requiring new protein synthesis and remained for the entire duration of RA treatment but rapidly reversed upon withdrawal of RA. A delayed protection observed at the initiator site was also reversed upon RA withdrawal. The RA-inducible footprint was not due to induction of factors that bind to these element, since in vitro assays showed that these factors are present in P19 cell extracts before RA treatment. Significantly, no RA-induced footprint was observed at any of these elements in P19 cells expressing a dominant negative RXR beta, in which RXR heterodimers are unable to bind to the beta RARE. Results indicate that binding of a liganded heterodimer receptor to the beta RARE is the initial event that allows other elements to gain access to the factors. In accordance, reporter analyses showed that a mutation in the beta RARE, but not those in other elements, abrogates RA activation of the promoter. It is likely that the RAR beta 2 promoter opens in a hierarchically ordered manner, signalled by the occupancy of liganded heterodimers.
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