The DOI matches its Crossref record; 71 of the 71 references it cites were found in a registry or an index.
Coregulators in Nuclear Estrogen Receptor Action: From Concept to Therapeutic Targeting
Abstract
Estrogens are key regulators of growth, differentiation, and the physiological functions of a wide range of target tissues, including the male and female reproductive tracts, breast, and skeletal, nervous, cardiovascular, digestive and immune systems. The majority of these biological activities of estrogens are mediated through two genetically distinct receptors, ERalpha and ERbeta, which function as hormone-inducible transcription factors. Over the past decade, it has become increasingly clear that the recruitment of coregulatory proteins to ERs is required for ER-mediated transcriptional and biological activities. These "coactivator" complexes enable the ERs to respond appropriately: 1) to hormones or pharmacological ligands, 2) interpret extra- and intra-cellular signals, 3) catalyze the process of chromatin condensation and 4) to communicate with the general transcription apparatus at target gene promoters. In addition to activating proteins, the existence of corepressors, proteins that function as negative regulators of ER activity in either physiological or pharmacological contexts, provides an additional level of complexity in ER action. This review also describes current efforts aimed at developing pharmaceutical agents that target ER-cofactor interactions as therapeutics for estrogen-associated pathologies.
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1 retracted
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Cited by
Vascular Actions of Estrogens: Functional Implications
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International Union of Pharmacology. LXIV. Estrogen Receptors
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Cracking the Estrogen Receptor's Posttranslational Code in Breast Tumors
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Metadata
- Authors
- Hall, J. M.
- Venue
- Molecular Interventions
- Publisher
- CLOCKSS Archive
- Published
- 2005-12-01
- Volume
- 5
- Issue
- 6
- Pages
- 343-357
- ISSN
- 1534-0384 (ISSN-L)
- OpenAlex
- W2067980525
- Cited by
- 295
- References
- 71
- FWCI
- 10.42
- Type
- journal article
- Language
- en
- Open access
- closed
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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