The DOI matches its OpenAlex record; 73 of the 73 references it cites were found in a registry or an index.
The Estrogen Receptor Enhances AP-1 Activity by Two Distinct Mechanisms with Different Requirements for Receptor Transactivation Functions
Open accessAbstract
Estrogen receptors (ERs alpha and beta) enhance transcription in response to estrogens by binding to estrogen response elements (EREs) within target genes and utilizing transactivation functions (AF-1 and AF-2) to recruit p160 coactivator proteins. The ERs also enhance transcription in response to estrogens and antiestrogens by modulating the activity of the AP-1 protein complex. Here, we examine the role of AF-1 and AF-2 in ER action at AP-1 sites. Estrogen responses at AP-1 sites require the integrity of the ERalpha AF-1 and AF-2 activation surfaces and the complementary surfaces on the p160 coactivator GRIP1 (glucocorticoid receptor interacting protein 1), the NID/AF-1 region, and NR boxes. Thus, estrogen-liganded ERalpha utilizes the same protein-protein contacts to transactivate at EREs and AP-1 sites. In contrast, antiestrogen responses are strongly inhibited by ERalpha AF-1 and weakly inhibited by AF-2. Indeed, ERalpha truncations that lack AF-1 enhance AP-1 activity in the presence of antiestrogens, but not estrogens. This phenotype resembles ERbeta, which naturally lacks constitutive AF-1 activity. We conclude that the ERs enhance AP-1 responsive transcription by distinct mechanisms with different requirements for ER transactivation functions. We suggest that estrogen-liganded ER enhances AP-1 activity via interactions with p160s and speculate that antiestrogen-liganded ER enhances AP-1 activity via interactions with corepressors.
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Cites
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Cited by
Estrogen receptors: how do they signal and what are their targets
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Molecular mechanism of estrogen–estrogen receptor signaling
Yaşar, P., Ayaz, G., User, S. D., Güpür, G., & Muyan, M. (2017) · Reproductive Medicine and Biology · doi:10.1002/rmb2.12006 · Cited by 482
Genomic Targets of Nuclear Estrogen Receptors
O’Lone, R., Frith, M. C., Karlsson, E. K., & Hansen, U. (2004) · Molecular Endocrinology · doi:10.1210/me.2003-0044 · Cited by 441
Safe, S., & Kim, K. (2008) · Journal of Molecular Endocrinology · doi:10.1677/jme-08-0103 · Cited by 368
Metadata
- Authors
- Webb, P. M., Nguyen, P. T., Valentine, C. D., Lopez, G. N., Kwok, G. R., McInerney, E. M., Katzenellenbogen, B. S., Enmark, E., Gustafsson, J.-Α., Nilsson, S. V., & Kushner, P. J.
- Venue
- Molecular Endocrinology
- Publisher
- Oxford University Press
- Published
- 1999-10-01
- Volume
- 13
- Issue
- 10
- Pages
- 1672-1685
- ISSN
- 0888-8809 (ISSN-L)
- OpenAlex
- W2100907853
- Cited by
- 396
- References
- 73
- FWCI
- 16.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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- CoChat. (2026). Citation check: The Estrogen Receptor Enhances AP-1 Activity by Two Distinct Mechanisms with Different Requirements for Receptor Transactivation Functions. https://app.cochat.ai/papers/10.1210/me.13.10.1672
- The paper
- Webb, P. M., Nguyen, P. T., Valentine, C. D., Lopez, G. N., Kwok, G. R., McInerney, E. M., Katzenellenbogen, B. S., Enmark, E., Gustafsson, J.-Α., Nilsson, S. V., & Kushner, P. J. (1999). The Estrogen Receptor Enhances AP-1 Activity by Two Distinct Mechanisms with Different Requirements for Receptor Transactivation Functions. Molecular Endocrinology. https://doi.org/10.1210/me.13.10.1672
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
