國家衛生研究院 NHRI:Item 3990099045/6818
English  |  正體中文  |  简体中文  |  全文筆數/總筆數 : 12145/12927 (94%)
造訪人次 : 857164      線上人數 : 251
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU 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
    主頁登入上傳說明關於NHRI管理 到手機版
    請使用永久網址來引用或連結此文件: http://ir.nhri.org.tw/handle/3990099045/6818


    題名: TLR9-mediated ARF6 activation is involved in advancing CpG ODN cellular uptake
    作者: Wu, JY;Kuo, CC
    貢獻者: Institute of Cellular and Systems Medicine
    摘要: Nucleic acid cellular uptake into endosomes is critical in eliciting nucleotide-sensing toll-like receptors (TLRs) innate immune responses. ADP-ribosylation factor 6 (ARF6) is a member of the Ras superfamily, which is critical to a wide variety of cellular events including endocytosis. Our previous report indicated that ARF6 plays a critical role in CpG ODN/TLR9-mediated responses. Here, we further explored that the basal level of active ARF6 is nonspecifically responsible for initiation of ODNs uptake, which is relatively CpG motif independent. While the initiation of CpG ODN uptake but not GpC ODN uptake can promote TLR9 responses thereby enhancing ARF6 activation which may lead to further nonspecifically increase of cellular uptake of stimulatory CpG ODN as well as nonstimulatory GpC ODN. Because nucleotide-sensing TLR9 plays a role in contributing to immune diseases, selective activation or inhibition of ARF6 might be useful in certain immunological or therapeutic applications.
    日期: 2012-07
    關聯: Communicative and Integrative Biology. 2012 Jul;5(4):316-318.
    Link to: http://dx.doi.org/10.4161/cib.20182
    Cited Times(Scopus): http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=84869831987
    顯示於類別:[郭呈欽] 期刊論文

    文件中的檔案:

    檔案 描述 大小格式瀏覽次數
    PUB23060951.pdf395KbAdobe PDF489檢視/開啟


    在NHRI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 IR team Copyright ©   - 回饋