English  |  正體中文  |  简体中文  |  Items with full text/Total items : 51296/86402 (59%)
Visitors : 8153163      Online Users : 121
RC Version 7.0 © Powered By DSPACE, MIT. Enhanced by NTU Library & TKU Library IR team.
Scope Tips:
  • please add "double quotation mark" for query phrases to get precise results
  • please goto advance search for comprehansive author search
  • Adv. Search
    HomeLoginUploadHelpAboutAdminister Goto mobile version
    Please use this identifier to cite or link to this item: http://tkuir.lib.tku.edu.tw:8080/dspace/handle/987654321/91702


    Title: Amikacin-induced Fin Reduction is Mediated by Autophagy
    Authors: Tsai, I-Ting;Chen, Yau-Hung;Wang, Yun-Hsin
    Contributors: 淡江大學生命科學研究所
    Keywords: amikacin;autophagy;embryotoxicity;fin reduction;zebrafish
    Date: 2013-03-01
    Issue Date: 2013-07-29 09:22:45 (UTC+8)
    Publisher: Tokyo: Japanese Society of Toxicologic Pathology
    Abstract: 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.
    Relation: Journal of Toxicologic Pathology 26(1), pp.79-82
    DOI: 10.1293/tox.26.79
    Appears in Collections:[化學學系暨研究所] 期刊論文

    Files in This Item:

    File Description SizeFormat
    2013 JTP.pdf887KbAdobe PDF550View/Open
    index.html0KbHTML282View/Open
    index.html0KbHTML5View/Open

    All items in 機構典藏 are protected by copyright, with all rights reserved.


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