A Novel Genetic System for Analysis of Co-activators for the N-Terminal Transactivation Function Domain of the Human Androgen Receptor

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  • TAKEYAMA Ken-ichi
    Institute of Molecular and Cellular Biosciences, University of Tokyo Solution Oriented Research for Science and Technology (SORST), Japan Science and Technology Agency (JST)
  • ITO Saya
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • SAWATSUBASHI Shun
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • SHIRODE Yuko
    Institute of Molecular and Cellular Biosciences, University of Tokyo Solution Oriented Research for Science and Technology (SORST), Japan Science and Technology Agency (JST)
  • YAMAMOTO Ayako
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • SUZUKI Eriko
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • MAKI Akio
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • YAMAGATA Kaoru
    Institute of Molecular and Cellular Biosciences, University of Tokyo Solution Oriented Research for Science and Technology (SORST), Japan Science and Technology Agency (JST)
  • ZHAO Yue
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • KOUZMENKO Alexandre
    Institute of Molecular and Cellular Biosciences, University of Tokyo Solution Oriented Research for Science and Technology (SORST), Japan Science and Technology Agency (JST)
  • TABATA Tetsuya
    Institute of Molecular and Cellular Biosciences, University of Tokyo
  • KATO Shigeaki
    Institute of Molecular and Cellular Biosciences, University of Tokyo Solution Oriented Research for Science and Technology (SORST), Japan Science and Technology Agency (JST)

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  • Novel Genetic System for Analysis of Co activators for the N Terminal Transactivation Function Domain of the Human Androgen Receptor

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Androgen receptor (hAR) regulates transcription of target genes in a ligand-dependent manner and recruits a number of co-activators for the ligand-induced transactivation via the N-terminal, activation function-1 (AF-1), and C-terminal, AF-2, transactivation domains. But the co-regulator functions on each of AR domains have not yet been fully understood. We have established a Drosophila transgenic system in which hAR and its deletion mutants are ectopically expressed in fly tissues together with an AR response element (ARE)-GFP reporter gene, and have confirmed that hAR was functional in ARE transactivation without affecting the expression of endogenous genes. We found that transcriptional activity of the hAR AF-1 domain was markedly reduced in Drosophila deficiency mutants of homologs for known mammalian co-activators of the AR ligand-dependent AF-2 domain. This suggests that hAR AF-1 recruits co-activators previously known only to interact with the AF-2 domain. Therefore, Drosophila with the hAR AF-1 transgene provides a relevant genetic system in which to uncover novel functions of vertebrate steroid hormone receptors and to screen for novel AF-1 co-regulators.

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