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Cited by 660Estrogen and related hormone effectsNuclear Receptors and SignalingGenomics and Chromatin Dynamics

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

Diverse signaling pathways modulate nuclear receptor recruitment of N-CoR and SMRT complexes.

Open access
Lavinsky, Robert M., Jepsen, Kristen, Heinzel, Thorsten, Torchia, Joseph, Mullen, Tina-Marie, Schiff, Rachel, Del-Rio, Alfonso Leon, Ricote, Mercedes, Ngo, Sally, Gemsch, Joslin, Hilsenbeck, Susan G., Osborne, C. Kent, Glass, Christopher K., Rosenfeld, Michael G., Rose, David W.·1998·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.95.6.2920PMC PMC19670
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Abstract

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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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
DOI
10.1073/pnas.95.6.2920
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
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

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