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Previous Volume 343:856-862 September 21, 2000 Number 12 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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Androgen-insensitivity syndromes in 46,XY fetuses result in various degrees of impairment in genital virilization.¹ These syndromes are caused by mutations in the androgen receptor gene that result in decreased binding of androgen to the receptor.^{2,3,4,5,6,7,8,9} As a consequence, the transcriptional activity of the androgen–androgen-receptor complex is reduced, and therefore, genital virilization is reduced. The androgen receptor, like other steroid hormone receptors, has two major transactivation domains¹⁰ — activation function 1 (AF-1) in the N-terminal region^11,12,13 and activation function 2 (AF-2) in the C-terminal ligand-binding domain¹⁴ — that interact with the target genes directly as well as indirectly by means of . . . [Full Text of this Article]

Case Report

Methods

Analysis of the Androgen Receptor

Plasmid Construction and Reporter Assay

Glutathione S-Transferase Assay

Results

Characterization of the Androgen Receptor

Activation of Transcription by the Androgen Receptor, the Glucocorticoid Receptor, Their Chimeras, and the Truncated Mutants

Electrophoretic Analysis of the Molecules Interacting with the AF-1 Region of the Androgen Receptor

Discussion

Source Information

From the Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Fukuoka (M.A., R.T., A.T., K.I., K.G., T.Y., S.I., H.N.); Core Research for Evolutional Science and Technology, Japan Science and Technology, Tokyo (R.T., K.G., T.Y., H.N.); and the Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo (S.K.) — all in Japan.

Address reprint requests to Dr. Nawata at the Department of Medicine and Bioregulatory Science, Graduate School of Medical Sciences, Kyushu University, Maidashi 3-1-1, Higashi-ku, Fukuoka 812-8582, Japan, or at nawata@intmed3.med.kyushu-u.ac.jp.

References

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