English  |  正體中文  |  简体中文  |  Items with full text/Total items : 90429/105609 (86%)
Visitors : 10325960      Online Users : 395
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTU 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://asiair.asia.edu.tw/ir/handle/310904400/16123


    Title: KEAP1 E3 ligase-mediated down regulation of NF-B signaling by targeting IKK.
    Authors: Lee, D-F;Kuo, H-P;Liu, M;Chou, C-K;Xia, W;Du, Y.;Shen, J;Chen, C-T;Huo, L;Hsu, M-C;Li, C-W;Ding, Q;Liao, T-L;Lai, C-C;Lin, A-C;Chang, Y-H;Tsai, S-F;李龍緣;Li, Long-Yuan;洪明奇;Hung, Mien-Chie
    Contributors: 生物科技學系
    Date: 2009
    Issue Date: 2012-11-23 17:08:50 (UTC+8)
    Abstract: IkappaB kinase beta (IKKbeta) is involved in tumor development and progression through activation of the nuclear factor (NF)-kappaB pathway. However, the molecular mechanism that regulates IKKbeta degradation remains largely unknown. Here, we show that a Cullin 3 (CUL3)-based ubiquitin ligase, Kelch-like ECH-associated protein 1 (KEAP1), is responsible for IKKbeta ubiquitination. Depletion of KEAP1 led to the accumulation and stabilization of IKKbeta and to upregulation of NF-kappaB-derived tumor angiogenic factors. A systematic analysis of the CUL3, KEAP1, and RBX1 genomic loci revealed a high percentage of genome loss and missense mutations in human cancers that failed to facilitate IKKbeta degradation. Our results suggest that the dysregulation of KEAP1-mediated IKKbeta ubiquitination may contribute to tumorigenesis.
    Relation: MOLECULAR CELL, V036 N.1:131–140.
    Appears in Collections:[生物科技學系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML209View/Open


    All items in ASIAIR are protected by copyright, with all rights reserved.


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