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- W2026540294 endingPage "7077" @default.
- W2026540294 startingPage "7066" @default.
- W2026540294 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." @default.
- W2026540294 created "2016-06-24" @default.
- W2026540294 creator A5022441204 @default.
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- W2026540294 date "1998-12-01" @default.
- W2026540294 modified "2023-10-18" @default.
- W2026540294 title "The hepatitis B virus X protein activates nuclear factor of activated T cells (NF-AT) by a cyclosporin A-sensitive pathway" @default.
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- W2026540294 doi "https://doi.org/10.1093/emboj/17.23.7066" @default.
- W2026540294 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/1171054" @default.
- W2026540294 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9843511" @default.
- W2026540294 hasPublicationYear "1998" @default.
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