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タイトル
  • en Co-localization with DJ-1 is essential for the androgen receptor to exert its transcription activity that has been impaired by androgen antagonists.
作成者
アクセス権 open access
主題
  • Other en DJ-1
  • Other en androgen receptor
  • Other en endocrine disrupter
  • MeSH en Androgen Antagonists/pharmacology
  • MeSH en Androgen Receptor Antagonists
  • MeSH en Animals
  • MeSH en COS Cells
  • MeSH en Cercopithecus aethiops
  • MeSH en Fluorescent Antibody Technique, Indirect
  • MeSH en Humans
  • MeSH en Oncogene Proteins/metabolism
  • MeSH en Oncogene Proteins/physiology
  • MeSH en Receptors, Androgen/metabolism
  • MeSH en Receptors, Androgen/physiology
  • MeSH en Transcription, Genetic
  • NDC 499
内容注記
  • Abstract en DJ-1 was first identified as a novel candidate of an oncogene product in cooperation with an activated ras, and DJ-1 was later found to be a positive regulator of the androgen receptor (AR) transcription activity that was repressed by PIASxalpha. DJ-1 was also found to be an infertility-related protein that was reduced in rat sperm treated with sperm toxicants that cause infertility in rats. To determine the roles of DJ-1 in the AR function, the effects of several androgen antagonists, some of which had been identified as endocrine-disrupting chemicals, on AR transcription activity and localization of AR and DJ-1 in Cos7 cells were examined. Co-localization of DJ-1 with the AR as dot-like spots in the nucleus was first found in cells that had not been treated with chemicals. Although all of the chemicals tested inhibited AR transcription activity to an average of 25% of that without chemicals, there were two classes affecting the localization of the two proteins; one changes the AR from dot-like spots to diffuse spaces in the nucleus and the other still keeps the AR in the dot-like spots. The localization of DJ-1, on the other hand, was found to be dramatically changed by all of the chemicals, resulting in loss of co-localization with the AR. These results indicate that DJ-1 is an essential factor for the AR to exert its full activity.
出版者 en The Pharmaceutical Society of Japan
日付
    Issued2004-04
言語
  • eng
資源タイプ journal article
出版タイプ VoR
資源識別子 HDL http://hdl.handle.net/2115/53741
関連
  • isIdenticalTo DOI https://doi.org/10.1248/bpb.27.574
  • PMID 15056870
収録誌情報
    • PISSN 0918-6158
      • en Biological & pharmaceutical bulletin
      • 27 4 開始ページ574 終了ページ577
ファイル
コンテンツ更新日時 2023-07-26