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    NFκB2 p52 has a role in antiviral immunity through IKKε -dependent induction of Sp1 and IL-15


    Doyle, Sarah L. and Shirey, Kari Ann and McGettrick, Anne F. and Kenny, Elaine F. and Carpenter, Susan B. and Caffrey, Brian E. and Gardan, Siobhan and Quinn, Susan R. and Cammano, Jorge H. and Moynagh, Paul N. and Vogel, Stefani N. and O'Neill, Luke A. (2013) NFκB2 p52 has a role in antiviral immunity through IKKε -dependent induction of Sp1 and IL-15. Journal of Biological Chemistry. ISSN 0021-9258

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    Abstract

    In this study we describe a previously unreported function for NFκB2, an NFκB family transcription factor, in antiviral immunity. NFκB2 is induced in response to Poly(I:C), a mimic of viral dsRNA. Poly(I:C), acting via TLR3, induces p52- dependent transactivation of a reporter gene in a manner that requires the kinase activity of IKKε and the transactivating potential of RelA/p65. We identify a novel NFκB2 binding site in the promoter of the transcription factor Sp1 which is required for Sp1 gene transcription activated by Poly(I:C). We show that Sp1 is required for IL-15 induction by both Poly(I:C) and Respiratory Syncitial Virus, a response that also requires NFκB2 and IKKε. Our study identifies NFκB2 as a target for IKKε in anti -viral immunity and describes, for the first time, a role for NFκB2 in the regulation of gene expression in response to viral infection.

    Item Type: Article
    Keywords: NFκB2; IKKε; p65; TLR3; RSV; Sp1; IL -15;
    Academic Unit: Faculty of Science and Engineering > Biology
    Item ID: 4967
    Identification Number: https://doi.org/10.1074/jbc.M113.469122
    Depositing User: Professor Paul Moynagh
    Date Deposited: 19 May 2014 14:32
    Journal or Publication Title: Journal of Biological Chemistry
    Publisher: American Society for Biochemistry and Molecular Biology
    Refereed: Yes
    URI:
    Use Licence: This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available here

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