淡江大學機構典藏:Item 987654321/91702
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 62805/95882 (66%)
造訪人次 : 3930815      線上人數 : 640
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library & TKU Library IR team.
搜尋範圍 查詢小技巧:
  • 您可在西文檢索詞彙前後加上"雙引號",以獲取較精準的檢索結果
  • 若欲以作者姓名搜尋,建議至進階搜尋限定作者欄位,可獲得較完整資料
  • 進階搜尋
    請使用永久網址來引用或連結此文件: https://tkuir.lib.tku.edu.tw/dspace/handle/987654321/91702


    題名: Amikacin-induced Fin Reduction is Mediated by Autophagy
    作者: Tsai, I-Ting;Chen, Yau-Hung;Wang, Yun-Hsin
    貢獻者: 淡江大學生命科學研究所
    關鍵詞: amikacin;autophagy;embryotoxicity;fin reduction;zebrafish
    日期: 2013-03-01
    上傳時間: 2013-07-29 09:22:45 (UTC+8)
    出版者: Tokyo: Japanese Society of Toxicologic Pathology
    摘要: Despite its medical use, little is known about the mechanisms underlying amikacin-induced embryotoxicity, including fin reduction, in zebrafish. In this study, we examined the expression of well-known autophagy markers mTOR (target of rapamycin), atg10 (autophagy-related gene), atg12 and LC3 (mammalian homolog of Atg8) in amikacin-treated zebrafish embryos. Our results indicated that the mRNA expression level of atg12 in the amikacin-treated group was significantly increased by 1.5-fold (p<0.05) compared with the corresponding mock control group, while the expression levels of atg10 and mTOR were significantly decreased by 0.74-fold (p<0.05) and 0.58-fold (p<0.05), respectively. Western blot analysis revealed that LC3 protein expression was induced by amikacin. Taken together, these data suggest that amikacin-induced fin reduction is mediated by fin cell autophagy.
    關聯: Journal of Toxicologic Pathology 26(1), pp.79-82
    DOI: 10.1293/tox.26.79
    顯示於類別:[化學學系暨研究所] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    2013 JTP.pdf887KbAdobe PDF628檢視/開啟
    index.html0KbHTML395檢視/開啟
    index.html0KbHTML111檢視/開啟

    在機構典藏中所有的資料項目都受到原著作權保護.

    TAIR相關文章

    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library & TKU Library IR teams. Copyright ©   - 回饋