NDLI: Genomic responses from the estrogen-responsive element-dependent signaling pathway mediated by estrogen receptor alpha are required to elicit cellular alterations.

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Genomic responses from the estrogen-responsive element-dependent signaling pathway mediated by estrogen receptor alpha are required to elicit cellular alterations.

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Genomic responses from the estrogen-responsive element-dependent signaling pathway mediated by estrogen receptor alpha are required to elicit cellular alterations.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Nott, Stephanie L. Welshons, Wade V. Huang, Yanfang Fluharty, Brian R. Qiu, Xing Li, Xiaodong Yeh, Shuyuan Muyan, Mesut
Description	Author Affiliation: Nott SL ( Department of Biochemistry and Biophysics, University of Rochester Medical School, Rochester, New York 14642, USA.)
Abstract	Estrogen (E2) signaling is conveyed by the transcription factors estrogen receptor (ER) alpha and beta. ERs modulate the expression of genes involved in cellular proliferation, motility, and death. The regulation of transcription by E2-ERalpha through binding to estrogen-responsive elements (EREs) in DNA constitutes the ERE-dependent signaling pathway. E2-ERalpha also modulates gene expression by interacting with transregulators bound to cognate DNA-regulatory elements, and this regulation is referred to as the ERE-independent signaling pathway. The relative importance of the ERE-independent pathway in E2-ERalpha signaling is unclear. To address this issue, we engineered an ERE-binding defective ERalpha mutant (ERalpha(EBD)) by changing residues in an alpha-helix of the protein involved in DNA binding to render the receptor functional only through the ERE-independent signaling pathway. Using recombinant adenovirus-infected ER-negative MDA-MB-231 cells derived from a breast adenocarcinoma, we found that E2-ERalpha(EBD) modulated the expression of a subset of ERalpha-responsive genes identified by microarrays and verified by quantitative PCR. However, E2-ERalpha(EBD) did not affect cell cycle progression, cellular growth, death, or motility in contrast to E2-ERalpha.ERalpha(EBD) in the presence of E2 was also ineffective in inducing phenotypic alterations in ER-negative U-2OS cells derived from an osteosarcoma. E2-ERalpha, on the other hand, effectively repressed growth in this cell line. Our findings suggest that genomic responses from the ERE-dependent signaling pathway are required for E2-ERalpha to induce alterations in cellular responses.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	22
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-05-29
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Estrogen Receptor Alpha Metabolism Estrogens Pharmacology Genome, Human Genetics Response Elements Signal Transduction Drug Effects Amino Acid Sequence Animals Cell Cycle Cell Death Cell Line Cell Movement Cell Nucleus Cell Proliferation DNA Chemistry Gene Expression Regulation Molecular Sequence Data Mutant Proteins Protein Binding Protein Structure, Tertiary Transcription, Genetic Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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