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Submitted on August 23, 2004
Accepted on October 20, 2004
Departments of Anatomy & Cell Biology, Obstetrics & Gynecology (I.S.N., A.A.T., V.K., C.D.L., C.D.T.-A.), and Neurology (C.D.T.-A.) and the Centers for Neurobiology and Behavior and Reproductive Sciences (I.S.N., A.A.T., V.K., C.D.L., C.D.T-A.), Columbia University College of Physicians & Surgeons, New York, New York 10032.
* To whom correspondence should be addressed. E-mail: cdt2{at}columbia.edu.
CHO-K1, COS-7 and Rat2 fibroblast cell lines are generally believed to be devoid of estrogen receptors (ERs) and have been widely used to study the functions of ER-
and ER-
following transfection of their cDNAs. Numerous studies have demonstrated that transfected ER- or ER- mediates estradiol-induced activation of multiple signaling pathways, including the mitogen-activated protein kinase/extracellular signal-regulated protein kinase pathways (MAPK/ERK). We report here for the first time that both 17-estradiol and 17-estradiol elicit activation of MAPK/ERK in native, non-transfected CHO-K1, COS-7 and Rat2 fibroblast cell lines. We further report that, contrary to the generally held belief, these cell lines are not unresponsive to estradiol in their native, non-transfected state, and that this estrogen responsiveness is associated with estrogen binding. Using multiple estrogen receptor antibodies, we failed to find ER-, ER- isoforms or even "ER-X". In view of these findings, researchers, using such cells as models to investigate mechanisms of estrogen action, must always take into account the existence of endogenous estrogen binding proteins other than ER-, ER- or "ER-X".
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