The DOI matches its Crossref record; 40 of the 41 references it cites were found in a registry or an index.
Reprogramming the Chromatin Landscape: Interplay of the Estrogen and Glucocorticoid Receptors at the Genomic Level
Open accessPublished version of a preprint
Abstract
Cross-talk between estrogen receptors (ER) and glucocorticoid receptors (GR) has been shown to contribute to the development and progression of breast cancer. Importantly, the ER and GR status in breast cancer cells is a significant factor in determining the outcome of the disease. However, mechanistic details defining the cellular interactions between ER and GR are poorly understood. We investigated genome-wide binding profiles for ER and GR upon coactivation and characterized the status of the chromatin landscape. We describe a novel mechanism dictating the molecular interplay between ER and GR. Upon induction, GR modulates access of ER to specific sites in the genome by reorganization of the chromatin configuration for these elements. Binding to these newly accessible sites occurs either by direct recognition of ER response elements or indirectly through interactions with other factors. The unveiling of this mechanism is important for understanding cellular interactions between ER and GR and may represent a general mechanism for cross-talk between nuclear receptors in human disease. Cancer Res; 73(16); 5130–9. ©2013 AACR.
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“Assisted loading has been described in various systems30–37.”
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The Human Genome Browser at UCSC
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Self-citationFOXA1 is a key determinant of estrogen receptor function and endocrine response
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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
Self-citationActivation of the ovalbumin gene by the estrogen receptor involves the Fos-Jun complex
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Metadata
- Authors
- Miranda, T. B., Voss, T. C., Sung, M.-H., Baek, S., John, S., Hawkins, M., Grøntved, L., Schiltz, R. L., & Hager, G. L.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Hager, Gordon L.
- Venue
- Cancer Research
- Published
- 2013-08-13
- Volume
- 73
- Issue
- 16
- Pages
- 5130-5139
- ISSN
- 0008-5472 (ISSN-L)
- 1538-7445
- PMC
- PMC3799864
- OpenAlex
- W2109796629
- Cited by
- 130
- References
- 41
- Citations by year
- 2026: 4 · 2025: 7 · 2024: 9 · 2023: 10 · 2022: 8 · 2021: 15 · 2020: 6 · 2019: 14 · 2018: 13 · 2017: 14 · 2016: 10 · 2015: 7 · 2014: 9 · 2013: 4
- FWCI
- 6.63
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Cancer Research (publishedVersion)
- PubMed (publishedVersion)
- University of Southern Denmark Research Portal (University of Southern Denmark) (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Lundbeckfonden
- National Institutes of Health
- National Cancer Institute (Z01BC005450)
- National Institute of General Medical Sciences
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Keywords
- estrogen receptor, glucocorticoid receptor, chromatin accessibility, chromatin reorganization, breast cancer, transcriptional regulation
- MeSH terms
- Animals, Binding Sites, Cell Line, Chromatin, DNA, Protein Binding, Receptors, Estrogen, Receptors, Glucocorticoid, Genome, Response Elements, Mice
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