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Diverse signaling pathways modulate nuclear receptor recruitment of N-CoR and SMRT complexes.
Open accessAbstract
Several lines of evidence indicate that the nuclear receptor corepressor (N-CoR) complex imposes ligand dependence on transcriptional activation by the retinoic acid receptor and mediates the inhibitory effects of estrogen receptor antagonists, such as tamoxifen, suppressing a constitutive N-terminal, Creb-binding protein/coactivator complex-dependent activation domain. Functional interactions between specific receptors and N-CoR or SMRT corepressor complexes are regulated, positively or negatively, by diverse signal transduction pathways. Decreased levels of N-CoR correlate with the acquisition of tamoxifen resistance in a mouse model system for human breast cancer. Our data suggest that N-CoR- and SMRT-containing complexes act as rate-limiting components in the actions of specific nuclear receptors, and that their actions are regulated by multiple signal transduction pathways.
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“Since then, it has been shown to be a corepressor molecule for androgen and estrogen receptors (19 -21).”
From The Nuclear Receptor Corepressor Has Organizational Effects within the Developing Amygdala on Juvenile Social Play and Anxiety-Like Behavior (2010) · cites this paper as [21]
In the citing paper
“Because NCoR appears to interact with both androgen (19,20) and estrogen receptors (21), it is possible that reducing NCoR expression enhances the function of both nuclear receptors to further masculinize juvenile social play.”
From The Nuclear Receptor Corepressor Has Organizational Effects within the Developing Amygdala on Juvenile Social Play and Anxiety-Like Behavior (2010) · cites this paper as [21]
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Background
Metadata
- Authors
- Lavinsky, R. M., Jepsen, K., Heinzel, T., Torchia, J., Mullen, T.-M., Schiff, R., Del-Rio, A. L., Ricote, M., Ngo, S., Gemsch, J., Hilsenbeck, S. G., Osborne, C. K., Glass, C. K., Rosenfeld, M. G., & Rose, D. W.
- Affiliations
- Howard Hughes Medical Institute (US)
- Howard Hughes Medical Institute, Cellular and Molecular Medicine, Whittier Diabetes Program, and UCSD Graduate Program in Biology, Department and School of Medicine, University of California at San Diego, La Jolla, CA 92093-0648; and Department of Medicine, Division of Medical Oncology, University of Texas Health Science Center at San Antonio, San Antonio, TX 78284-7884
- Corresponding author
- Rose, David W.
- ORCID
- Venue
- Proceedings of the National Academy of Sciences
- Publisher
- National Academy of Sciences
- Published
- 1998-03-17
- Volume
- 95
- Issue
- 6
- Pages
- 2920-2925
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- PMC
- PMC19670
- OpenAlex
- W2128003724
- Cited by
- 660
- References
- 52
- Citations by year
- 2026: 5 · 2025: 2 · 2024: 6 · 2023: 3 · 2022: 10 · 2021: 6 · 2020: 10 · 2019: 13 · 2018: 10 · 2017: 11 · 2016: 13 · 2015: 15 · 2014: 13 · 2013: 12 · 2012: 20
- FWCI
- 30.37
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Proceedings of the National Academy of Sciences (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Science Foundation
- Howard Hughes Medical Institute
- American Diabetes Association
- National Institutes of Health
- National Cancer Institute (P30CA 54174, P30CA054174, P50 CA58183, P50CA058183)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Genomics and Chromatin Dynamics
- Keywords
- nuclear receptor corepressor, SMRT, signaling pathways, retinoic acid receptor, estrogen receptor, tamoxifen resistance, breast cancer, transcriptional repression, ligand-dependent transcription, CREB-binding protein, coactivator complexes
- MeSH terms
- Animals, Breast Neoplasms, Disease Models, Animal, DNA-Binding Proteins, Drug Resistance, Estrogen Antagonists, Gene Expression Regulation, Humans, Models, Biological, Nuclear Proteins, Protein Binding, Protein Kinases, Receptors, Estrogen, Repressor Proteins, Tamoxifen, Signal Transduction, Genes, Reporter, Receptors, Retinoic Acid, Mice, Nuclear Receptor Co-Repressor 1, Nuclear Receptor Co-Repressor 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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