ArticleNucleic acids research1996
Differential transcriptional regulation of the apoAI gene by retinoic acid receptor homo- and heterodimers in yeast.
Article in Nucleic acids research, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 15 citations in OpenAlex.
- Retinoids increase human apo C-III expression at the transcriptional level via the retinoid X receptor. Contribution to the hypertriglyceridemic action of retinoids.The Journal of clinical investigation · 1998Trial
- Protein kinase D1 (PKD1) influences androgen receptor (AR) function in prostate cancer cells.Biochemical and biophysical research communications · 2008Article
- Apigenin suppresses cancer cell growth through ERbeta.Neoplasia (New York, N.Y.) · 2006Article
- Estrogen receptor (ER)-beta isoforms: a key to understanding ER-beta signaling.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- A yeast screen system for aromatase inhibitors and ligands for androgen receptor: yeast cells transformed with aromatase and androgen receptor.Environmental health perspectives · 1999Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Several members of the nuclear receptor superfamily including RXR (retinoid X receptor) bind to a specific retinoic acid response element (site A) of the apoAI promoter. However, transcriptional activation of the apoAI gene by different homo- and heterodimeric forms of RXR or RAR (retinoic acid receptors) cannot be evaluated in mammalian cells, which contain endogenous RXR or RAR. In order to circumvent this limitation, we assessed the DNA-binding activities and transcriptional activation of different homo- and heterodimers of these receptors in yeast. Electrophoretic mobility shift assays (EMSA) demonstrated that yeast expressed RARalpha does not bind to site A of the apoAl promoter, whereas binding of RARbeta to site A is ligand-dependent. Both RARalpha and RARbeta form heterodimers with RXRalpha and bind to site A with high affinity. These DNA-binding studies correlate with the transcriptional data, which indicated that RARbeta but not RARalpha activates transcription from site A in response equally well to 9-cis and all-trans retinoic acids. 9-cis RA is a more potent ligand than all-trans RA to activate transcription via RXR/RAR heterodimers. We conclude that this yeast expression system is a useful tool to elucidate the 'transactivation code' for apoAl site A via specific combinations of different homo and heterodimeric versions of RXR and RAR.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.