© 2005 The Japanese Biochemical Society
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Study of Androgen Receptor Functions by Genetic Models
1 Institute of Molecular and Cellular Biosciences, University of Tokyo, 1-1-1 Yayoi, Bunkyo-ku, Tokyo, 113-0032; and 2 ERATO, Japan Science and Technology Agency, 4-1-8 Honcho, Kawaguchi, Saitama, 332-0012
* To whom correspondence should be addressed at: Institute of Molecular and Cellular Biosciences, University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-0032. Fax: +81-3-5841-8477, Tel: +81-3-5841-8478, E-mail: uskato{at}mail.ecc.u-tokyo.ac.jp
Androgens exert most of their biological activities through binding to the androgen receptor (AR). The AR belongs to the nuclear receptor superfamily and acts as a ligand-inducible transcriptional factor. AR dysfunction causes a diverse range of clinical conditions, such as testicular mutation (Tfm) syndrome, prostate cancer, and spinal and bulbar muscular atrophy (SBMA). However, the molecular basis of the AR function underlying these AR-related disorders remains largely unknown due to the lack of stable genetic models. Here we review recent results of our studies into genetic models of the loss of AR function in mice and the gain of AR function in Drosophila.
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