ArticleMolecular and cellular biology1994
Dominant negative retinoid X receptor beta inhibits retinoic acid-responsive gene regulation in embryonal carcinoma cells.
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 17 papers.
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Who cites it
17 citing papers in PubMed, 66 citations in OpenAlex.
- Retinoid signaling in inner ear development: A "Goldilocks" phenomenon.American journal of medical genetics. Part A · 2010Review
- All trans retinoic acid nanodisks enhance retinoic acid receptor mediated apoptosis and cell cycle arrest in mantle cell lymphoma.British journal of haematology · 2010Article
- Design and synthesis of novel derivatives of all-trans retinoic acid demonstrate the combined importance of acid moiety and conjugated double bonds in its binding to PML-RAR-alpha oncogene in acute promyelocytic leukemia.Leukemia & lymphoma · 2010Article
- The methyl-CpG binding protein MBD1 is required for PML-RARalpha function.Proceedings of the National Academy of Sciences of the United States of America · 2006Article
- Chromosomal integration of retinoic acid response elements prevents cooperative transcriptional activation by retinoic acid receptor and retinoid X receptor.Molecular and cellular biology · 2002Article
- Article
- Leukemic transformation by the v-ErbA oncoprotein entails constitutive binding to and repression of an erythroid enhancer in vivo.The EMBO journal · 1998Article
- Synergistic transcriptional activation of the mouse urokinase plasminogen activator (uPA) gene and of its enhancer activator protein 1 (AP1) site by cAMP and retinoic acid.The Biochemical journal · 1998Article
- 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
- Transcriptional regulation of the Xlim-1 gene by activin is mediated by an element in intron I.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Retinoid X receptor (RXR) within the RXR-retinoic acid receptor heterodimer binds its ligand and enhances retinoid-dependent gene expression.Molecular and cellular biology · 1997Article
- Retinoid X receptor-selective ligands produce malformations in Xenopus embryos.Proceedings of the National Academy of Sciences of the United States of America · 1996Article
- Vesicular stomatitis virus infection induces a nuclear DNA-binding factor specific for the interferon-stimulated response element.Journal of virology · 1995Article
- Transcription factor TFIIB and the vitamin D receptor cooperatively activate ligand-dependent transcription.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Mouse retinoid X receptor contains a separable ligand-binding and transactivation domain in its E region.Molecular and cellular biology · 1995Article
- Ligand-dependent occupancy of the retinoic acid receptor beta 2 promoter in vivo.Molecular and cellular biology · 1994Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinoid X receptors (RXRs) heterodimerize with multiple nuclear hormone receptors and are thought to exert pleiotropic functions. To address the role of RXRs in retinoic acid- (RA) mediated gene regulation, we designed a dominant negative RXR beta. This mutated receptor, termed DBD-, lacked the DNA binding domain but retained the ability to dimerize with partner receptors, resulting in formation of nonfunctional dimers. DBD- was transfected into P19 murine embryonal carcinoma (EC) cells, in which reporters containing the RA-responsive elements (RAREs) were activated by RA through the activity of endogenous RXR-RA receptor (RAR) heterodimers. We found that DBD- had a dominant negative activity on the RARE reporter activity in these cells. P19 clones stably expressing DBD- were established; these clones also failed to activate RARE-driven reporters in response to RA. Further, these cells were defective in RA-induced mRNA expression of Hox-1.3 and RAR beta, as well as in RA-induced down-regulation of Oct3 mRNA. Gel mobility shift assays demonstrated that RA treatment of control P19 cells induces RARE-binding activity, of which RXR beta is a major component. However, the RA-induced binding activity was greatly reduced in cells expressing DBD-. By genomic footprinting, we show that RA treatment induces in vivo occupancy of the RARE in the endogenous RAR beta gene in control P19 cells but that this occupancy is not observed with the DBD- cells. These data provide evidence that the dominant negative activity of DBD- is caused by the lack of receptor binding to target DNA. Finally, we show that in F9 EC cells expression of DBD- leads to inhibition of the growth arrest that accompanies RA-induced differentiation. Taken together, these results demonstrate that RXR beta and partner receptors play a central role in RA-mediated gene regulation and in the control of growth and differentiation in EC cells.
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