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directly to, albeit weakly, and activates ER in T47Dco and HEK-293
cells. Transactivation in the former cells was mediated by ER as it
was completed abrogated by the antiestrogen ICI 182,780. This is
in agreement with our in vivo results showing induction by bolan-
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Furthermore, bolandiol stimulated transcription via ER in U2OS
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In conclusion, we have shown in this study that bolandiol
injected sc is effective in suppressing LH in castrated young rats
and in maintaining LA development while having less of a stimula-
tory effect on the prostate and SV than T. Bolandiol does not require
aromatization or 5␣-reduction to support these physiologic end-
points. The mechanism of action of bolandiol is likely through a
combination of AR, PR, and ER as it binds weakly to, but exhibits
transactivation of all these receptors, in contrast to T and E2. Future
experiments examining the effect of bolandiol in steroid receptor
knock-out mice may help to further clarify its mechanism of action.
Collectively, bolandiol has properties consistent with its charac-
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This work was supported by contract NIH NO1-HD-2-3338
awarded to BIOQUAL, Inc. and NIA Grant K23 AG027238-01 A1
awarded to STP. We would like to thank Dr. June Lee of the Contra-
ception and Reproductive Health Branch of NICHD, Project Officer
on the contract and Dr. Richard Blye, former Project Officer, for
their support, and Trung Pham, Laurent Pessaint, Jessica Pray, Jean
Engbring, Bruce Till, David Gropp and Anne Semon for technical
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