論文

査読有り
2021年9月26日

Isorhamnetin Promotes 53BP1 Recruitment through the Enhancement of ATM Phosphorylation and Protects Mice from Radiation Gastrointestinal Syndrome.

Genes
  • 西山 祐一
  • 森田 明典
  • Tatsuta Shogo
  • Kanamaru Misaki
  • Sakaue Masahiro
  • Ueda Kenta
  • Shono Manami
  • Fujita Rie
  • Wang Bing
  • Hosoi Yoshio
  • Aoki Shin
  • Sugai Takeshi
  • 全て表示

Vol.12
No.10
開始ページ
1514
終了ページ
1514
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.3390/genes12101514

Flavonoids are a subclass of polyphenols which are attractive, due to possessing various physiological activities, including a radioprotective effect. Tumor suppressor p53 is a primary regulator in the radiation response and is involved in the pathogenesis of radiation injuries. In this study, we revealed that isorhamnetin inhibited radiation cell death, and investigated its action mechanism focusing on DNA damage response. Although isorhamnetin moderated p53 activity, it promoted phosphorylation of ataxia telangiectasia mutated (ATM) and enhanced 53BP1 recruitment in irradiated cells. The radioprotective effect of isorhamnetin was not observed in the presence of ATM inhibitor, indicating that its protective effect was dependent on ATM. Furthermore, isorhamnetin-treated mice survived gastrointestinal death caused by a lethal dose of abdominal irradiation. These findings suggested that isorhamnetin enhances the ATM-dependent DNA repair process, which is presumably associated with the suppressive effect against GI syndrome.

リンク情報
DOI
https://doi.org/10.3390/genes12101514
URL
https://repo.lib.tokushima-u.ac.jp/ja/116406
URL
https://web.db.tokushima-u.ac.jp/cgi-bin/edb_browse?EID=382828
URL
https://www.ncbi.nlm.nih.gov/pubmed/34680909
ID情報
  • DOI : 10.3390/genes12101514
  • ISSN : 2073-4425
  • eISSN : 2073-4425

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