The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.
Genomic Antagonism between Retinoic Acid and Estrogen Signaling in Breast Cancer
Open accessAbstract
SUMMARY Retinoic acid (RA) triggers growth-suppressive effects in tumor cells and therefore RA has and its synthetic analogs have great potential as anti-carcinogenic agent. RA effects are mediated by Retinoic Acid Receptors (RARs), which regulate gene expression in an RA-dependent manner. To define the genetic network regulated by RARs in breast cancer, we identified RAR genomic targets using chromatin immunoprecipitation and expression analysis. We found that RAR binding throughout the genome is highly co-incident with estrogen receptor α (ERα) binding, and identified a widespread crosstalk of RA and estrogen signaling to antagonistically regulate breast cancer-associated genes. ERα and RAR binding sites appear to be co-evolved on a large scale throughout the human genome, allowing for competitive binding between these transcription factors via nearby or overlapping cis-regulatory elements. Together these data indicate the existence of a highly coordinated intersection between these two critical nuclear hormone receptor signaling pathways providing a global mechanism for balancing gene expression output via local regulatory interactions dispersed throughout the genome.
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Subramanian, A., Tamayo, P., Mootha, V. K., Mukherjee, S., Ebert, B. L., Gillette, M. A., Paulovich, A., Pomeroy, S. L., Golub, T. R., Lander, E. S., et al. (2005) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0506580102 · Cited by 53,625
Smyth, G. K. (2004) · Statistical Applications in Genetics and Molecular Biology · doi:10.2202/1544-6115.1027 · Cited by 11,829
A decade of molecular biology of retinoic acid receptors
Chambon, P. (1996) · The FASEB Journal · doi:10.1096/fasebj.10.9.8801176 · Cited by 2,889 · cited 2×
“…RARRXR heterodimers are thought to function primarily as transcriptional activators while repression is thought to be primarily mediated by unliganded heterodimers interfering with basal transcription (Chambon, 1996; Glass and Rosenfeld, 2000; Hu and Lazar, 2000; Niederreither andDolle, 2008).”
The coregulator exchange in transcriptional functions of nuclear receptors
Glass, C. K., & Rosenfeld, M. G. (2000) · Genes & Development · doi:10.1101/gad.14.2.121 · Cited by 2,233
A human retinoic acid receptor which belongs to the family of nuclear receptors
Petkovich, M., Brand, N. J., Krust, A., & Chambon, P. (1987) · Nature · doi:10.1038/330444a0 · Cited by 2,214
Identification of a receptor for the morphogen retinoic acid
Giguere, V., Ong, E. S., Segui, P., & Evans, R. M. (1987) · Nature · doi:10.1038/330624a0 · Cited by 1,965 · cited 2×
“Previous work has identified two subfamilies of nuclear receptors as major mediators of RA signaling, the retinoic acid receptors (RARs) and the retinoid X receptors (RXRs) (Evans, 1988; Giguere et al., 1987; Mangelsdorf and Evans, 1995; Petkovich et al., 1987).”
Gene expression regulation by retinoic acid
Balmer, J. E., & Blomhoff, R. (2002) · Journal of Lipid Research · doi:10.1194/jlr.r100015-jlr200 · Cited by 1,039
Retinoic acid in development: Towards an integrated view
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A module map showing conditional activity of expression modules in cancer
Segal, E., Friedman, N., Koller, D., & Regev, A. (2004) · Nature Genetics · doi:10.1038/ng1434 · Cited by 685
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Cited by
ChIP-seq guidelines and practices of the ENCODE and modENCODE consortia
Landt, S. G., Marinov, G. K., Kundaje, A., Kheradpour, P., Pauli, F., Batzoglou, S., Bernstein, B. E., Bickel, P., Brown, J. B., Cayting, P., et al. (2012) · Genome Research · doi:10.1101/gr.136184.111 · Cited by 2,033
Self-citationA vitamin D receptor/SMAD genomic circuit gates hepatic fibrotic response
Ding, N., Yu, R. T., Subramaniam, N., Sherman, M. H., Wilson, C., Rao, R., Leblanc, M., Coulter, S., He, M., Scott, C., et al. (2013) · Cell · doi:10.1016/j.cell.2013.03.028 · Cited by 622
Retinoids, Retinoic Acid Receptors, and Cancer
Tang, X.-H., & Gudas, L. J. (2011) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev-pathol-011110-130303 · Cited by 596
Transcription Factor AP1 Potentiates Chromatin Accessibility and Glucocorticoid Receptor Binding
Biddie, S. C., John, S., Sabo, P. J., Thurman, R. E., Johnson, T. A., Schiltz, R. L., Miranda, T. B., Sung, M.-H., Trump, S., Lightman, S. L., et al. (2011) · Molecular Cell · doi:10.1016/j.molcel.2011.06.016 · Cited by 503
Retinoids regulate stem cell differentiation
Gudas, L. J., & Wagner, J. A. (2011) · Journal of Cellular Physiology · doi:10.1002/jcp.22417 · Cited by 395
Metadata
- Authors
- Hua, S., Kittler, R., & White, K. P.
- Venue
- Cell
- Publisher
- Elsevier BV
- Published
- 2009-06
- Volume
- 137
- Issue
- 7
- Pages
- 1259-1271
- ISSN
- 0092-8674 (ISSN-L)
- OpenAlex
- W2080683349
- Cited by
- 307
- References
- 11
- FWCI
- 13.01
- Type
- journal article
- Language
- en
- Open access
- bronze
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