Endogenously Expressed Estrogen Receptor and Coactivator AIB1 Interact in MCF-7 Human Breast Cancer Cells
Coactivators are believed to mediate estrogen-induced gene responses via interaction with estrogen receptors (ER). Currently, a major challenge is to determine the importance of each coactivator in a specific cell type and promoter context in response to a particular ligand. The potential of ER to i...
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Published in | Proceedings of the National Academy of Sciences - PNAS Vol. 97; no. 23; pp. 12536 - 12540 |
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Main Authors | , , , , , , |
Format | Journal Article |
Language | English |
Published |
United States
National Academy of Sciences of the United States of America
07.11.2000
National Acad Sciences National Academy of Sciences The National Academy of Sciences |
Subjects | |
Online Access | Get full text |
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Summary: | Coactivators are believed to mediate estrogen-induced gene responses via interaction with estrogen receptors (ER). Currently, a major challenge is to determine the importance of each coactivator in a specific cell type and promoter context in response to a particular ligand. The potential of ER to interact with a growing list of coactivators has been shown in a variety of in vitro and gene transfer assays, yet very few data have demonstrated the interaction of endogenous coactivators with ER in intact cells. We report here a ligand-specific interaction of endogenous human ER (hER) and the AIB1 coactivator in MCF-7 human breast cancer cells by using immunoprecipitation analyses. Complexes between endogenously expressed hER and AIB1 were detected in estradiol-treated cells and to a much lesser extent in cells treated with the partial agonist, monohydroxytamoxifen. We were unable to detect an hER-SRC-1 complex in our immunoprecipitations from MCF-7 cells. The in vitro-binding affinity for mouse ER interaction with AIB1 was estimated to be 40-120 nM. We conclude that AIB1 is a major coactivator for hER in MCF-7 human breast cancer cells. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 To whom reprint requests should be addressed at: Department of Pathology and Laboratory Medicine, University of Wisconsin–Madison, MSC 5330, 1300 University Avenue, Madison, WI 53706. Previous address: Department of Biochemistry, Uniformed Services University of the Health Sciences, Bethesda, MD 20814. Communicated by Jack Gorski, University of Wisconsin, Madison, WI |
ISSN: | 0027-8424 1091-6490 |
DOI: | 10.1073/pnas.220427297 |