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    The hepatitis B virus X protein activates nuclear factor of activated T cells (NF-AT) by a cyclosporin A-sensitive pathway.

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    Authors
    Lara-Pezzi, Enrique
    Armesilla, Angel cc
    Majano, Pedro L.
    Redondo, Juan Miguel
    López-Cabrera, Manuel
    Issue Date
    1998-12-01
    
    Metadata
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    Abstract
    The X gene product of the human hepatitis B virus (HBx) is a transcriptional activator of various viral and cellular genes. We recently have determined that the production of tumor necrosis factor-alpha (TNF-alpha) by HBV-infected hepatocytes is transcriptionally up-regulated by HBx, involving nuclear factor of activated T cells (NF-AT)-dependent activation of the TNF-alpha gene promoter. Here we show that HBx activates NF-AT by a cyclosporin A-sensitive mechanism involving dephosphorylation and nuclear translocation of the transcription factor. Luciferase gene expression assays demonstrated that HBx transactivates transcription through NF-AT-binding sites and activates a Gal4-NF-AT chimeric protein. DNA-protein interaction assays revealed that HBx induces the formation of NF-AT-containing DNA-binding complexes. Immunofluorescence analysis demonstrated that HBx induces the nuclear translocation of NF-AT, which can be blocked by the immunosuppressive drug cyclosporin A. Furthermore, immunoblot analysis showed that the HBx-induced activation and translocation of NF-AT are associated with its dephosphorylation. Thus, HBx may play a relevant role in the intrahepatic inflammatory processes by inducing locally the expression of cytokines that are regulated by NF-AT.
    Citation
    The EMBO Journal, 17(23): 7066-7077
    Publisher
    Nature Publishing Group
    URI
    http://hdl.handle.net/2436/7705
    DOI
    10.1093/emboj/17.23.7066
    PubMed ID
    9843511
    Additional Links
    http://www.pubmedcentral.nih.gov/picrender.fcgi?artid=1171054&blobtype=pdf
    Type
    Journal article
    Language
    en
    ISSN
    0261-4189
    ae974a485f413a2113503eed53cd6c53
    10.1093/emboj/17.23.7066
    Scopus Count
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    Research Institute in Healthcare Science

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