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Modulation of Cell Proliferation and Gene Expression by a p53-Estrogen Receptor Hybrid Protein
Klaus Roemer and Theodore Friedmann
Proceedings of the National Academy of Sciences of the United States of America
Vol. 90, No. 20 (Oct. 15, 1993), pp. 9252-9256
Published by: National Academy of Sciences
Stable URL: http://www.jstor.org/stable/2363131
Page Count: 5
You can always find the topics here!Topics: Cell growth, Cell lines, Plasmids, Hormones, Cell cycle, Transactivation, Hybridity, Estrogen receptors, Transfection, DNA
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We report that p53her, a chimeric protein consisting of the complete human wild-type p53 and the human estrogen receptor hormone-binding domain, strongly suppresses proliferation and induces characteristic morphological changes in Saos-2 human osteosarcoma cells when induced by 17β-estradiol. In contrast, p53her constitutively transactivates a p53-responsive promoter in transfection assays, so that transactivation is not regulated by estradiol. However, coexpression of p53her and oncoprotein MDM-2, which associates with and presumably inactivates p53, results in suppression of p53her-mediated transactivation in the absence, but not the presence, of estradiol. Similarly, p53her induces expression of an endogenous MDM-2 transcript only in the presence of estradiol. These results suggest a correlation between the growth suppressor function of p53her and release of a transactivation block mediated by MDM-2.
Proceedings of the National Academy of Sciences of the United States of America © 1993 National Academy of Sciences