English  |  正體中文  |  简体中文  |  Items with full text/Total items : 54367/62174 (87%)
Visitors : 13860393      Online Users : 38
RC Version 6.0 © Powered By DSPACE, MIT. Enhanced by NTHU 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
    National Tsing Hua University Institutional Repository > 生命科學院  > 生命科學系 > 期刊論文 >  Activation of protein kinase Ca signaling prevents cytotoxicity and mutagenicity following lead acetate in CL3 human lung cancer cells


    Please use this identifier to cite or link to this item: http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/49405


    Title: Activation of protein kinase Ca signaling prevents cytotoxicity and mutagenicity following lead acetate in CL3 human lung cancer cells
    Authors: Wang CY;Lin YW;YangJL
    教師: 楊嘉鈴
    Date: 2008
    Publisher: Elsevier
    Relation: Toxicology,Elsevier,Volume 250,Issue 1,2008,Pages 55-61
    Keywords: Cancer
    Malignant tumor
    Lung disease
    Bronchus disease
    Respiratory disease
    Heavy metal
    Abstract: Protein kinase C (PKC) family of serine/threonine protein kinases is sensitive signaling transducers in response to lead acetate (Pb) that could transmit phosphorylation cascade for proliferation and de-differentiation of neural cells. However, little is known as to the impact of PKC on Pb genotoxicity. Here we investigate whether Pb activates the conventional/classical subfamily of PKC (cPKC) signaling to affect cytotoxicity and mutagenicity in CL3 human non-small-cell lung adenocarcinoma cells. Pb specifically promoted membrane localization of the a isoform of PKC in CL3 cells. Pb also elicited Raf-1 activation as measured by the induction of phospho-Raf-1S338 and the dissociation from the Raf-1 kinase inhibitor protein. Inhibition of cPKC activity using Gö6976 or depletion of PKCα by introducing specific small interfering RNA blocked the induction of phospho-Raf-1S338, phospho-MKK1/2 and phospho-ERK1/2 in cells exposed to Pb. Intriguingly, declining PKCa enhanced the Pb cytotoxicity and revealed the Pb mutagenicity at the hprt gene. The results suggest that PKCa is obligatory for activation of the Raf-1-MKK1/2-ERK1/2 signaling module and plays a defensive role against cytotoxicity and mutagenicity following Pb exposure. Results obtained in this study also support our previous report showing that ERK1/2 activity is involved in preventing Pb genotoxicity.
    URI: http://cat.inist.fr/?aModele=afficheN&cpsidt=20573119
    http://www.elsevier.com/
    http://nthur.lib.nthu.edu.tw/dspace/handle/987654321/49405
    Appears in Collections:[生命科學系] 期刊論文

    Files in This Item:

    File Description SizeFormat
    index.html0KbHTML1061View/Open


    在NTHUR中所有的資料項目都受到原著作權保護,僅提供學術研究及教育使用,敬請尊重著作權人之權益。若須利用於商業或營利,請先取得著作權人授權。
    若發現本網站收錄之內容有侵害著作權人權益之情事,請權利人通知本網站管理者(smluo@lib.nthu.edu.tw),管理者將立即採取移除該內容等補救措施。

    SFX Query

    與系統管理員聯絡

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