English  |  正體中文  |  简体中文  |  Post-Print筆數 : 27 |  Items with full text/Total items : 109874/140825 (78%)
Visitors : 45946005      Online Users : 803
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: https://nccur.lib.nccu.edu.tw/handle/140.119/70087

    Title: Brain-Derived Neurotrophic Factor Enhances Bcl-xL Expression Through Protein Kinase Casein Kinase 2-Activated and Nuclear Factor Kappa B-Mediated Pathway in Rat Hippocampus
    Authors: 趙知章
    Chao, Chih Chang;Chiang,CH;Ma,YL;Lee,EH
    Contributors: 神科所
    Keywords: Bcl-xL;brain-derived neurotrophic factor;casein kinase 2;hippocampus;neuroprotection;NF-kB
    Date: 2011.05
    Issue Date: 2014-09-23 12:25:04 (UTC+8)
    Abstract: Brain-derived neurotrophic factor (BDNF) was shown to produce its neuroprotective effect through extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphatidylinositol-3 kinase (PI3-K) signaling. But whether other pathways also mediate the neuroprotective effect of BDNF is less known. In this study, we found that direct administration of BDNF to rat hippocampal CA1 area dose-dependently increased the mRNA and protein levels of Bcl-xL. BDNF also increased protein kinase casein kinase II (CK2) activity and NF-kB phosphorylation at Ser529 dose-dependently. Further, transfection of the wild-type CK2a DNA to CA1 neurons increased nuclear factor kappa B (NF-kB) phosphorylation and Bcl-xL mRNA expression, whereas transfection of CK2a156A, the catalytically inactive mutant of CK2a, decreased these measures. Moreover, transfection of CK2a small interfering RNA (siRNA) blocked the enhancing effect of BDNF on NF-kB phosphorylation and Bcl-xL expression. These results were further confirmed by treatment of 4,5,6,7tetrabromobenzotriazole (TBB), a specific CK2 inhibitor. Transfection of NF-kBS529A, the dominant negative mutant of NF-kB, prevented the enhancing effect of BDNF on Bcl-xL expression. More importantly, BDNF activation of CK2 is not affected by co-administration of the ERK1/2 inhibitor, PD98059, and the PI3-K inhibitor, LY294002. These results demonstrate a novel BDNF signaling pathway and provide an alternative therapeutic strategy for the protective effect of BDNF on hippocampal neurons in vivo.
    Relation: Brain Pathology,21(2),150-162
    Data Type: article
    DOI 連結: http://dx.doi.org/10.1111/j.1750-3639.2010.00431.x
    DOI: 10.1111/j.1750-3639.2010.00431.x
    Appears in Collections:[神經科學研究所 ] 期刊論文

    Files in This Item:

    File Description SizeFormat
    150-062.pdf1079KbAdobe PDF21280View/Open

    All items in 政大典藏 are protected by copyright, with all rights reserved.

    社群 sharing

    著作權政策宣告 Copyright Announcement
    The digital content of this website is part of National Chengchi University Institutional Repository. It provides free access to academic research and public education for non-commercial use. Please utilize it in a proper and reasonable manner and respect the rights of copyright owners. For commercial use, please obtain authorization from the copyright owner in advance.

    NCCU Institutional Repository is made to protect the interests of copyright owners. If you believe that any material on the website infringes copyright, please contact our staff(nccur@nccu.edu.tw). We will remove the work from the repository and investigate your claim.
    DSpace Software Copyright © 2002-2004  MIT &  Hewlett-Packard  /   Enhanced by   NTU Library IR team Copyright ©   - Feedback