Regulatory RNA induces the production of IFN-g, but not IL-4 in human lymphocytes: Role of RNA-dependent protein inase (PKR) and NF-B

Previous results with p9-RNA, obtained from lymph nodes of animals immunized with the peptide p9 of HIV-1, suggested that its effects on lymphocytes could be mediated by RNA-dependent protein kinase (PKR). Here we report that p9-RNA activates PKR leading to the degradation of the inhibitor I-Ba and...

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Bibliographic Details
Published in:Molecular and cellular biochemistry 2003-05, Vol.247 (1-2), p.211-217
Main Authors: De Lucca, Fernando L, Sales, Valeria SF, Souza, Liliana R, Murad, Joana M, Watanabe, Maria Angelica E
Format: Article
Language:English
Subjects:
Human immunodeficiency virus 1
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Summary:Previous results with p9-RNA, obtained from lymph nodes of animals immunized with the peptide p9 of HIV-1, suggested that its effects on lymphocytes could be mediated by RNA-dependent protein kinase (PKR). Here we report that p9-RNA activates PKR leading to the degradation of the inhibitor I-Ba and the concomitant nuclear factor kappa B (NF-B) activation. The fractionation of p9-RNA by affinity chromatography indicates that the poly A(+) p9-RNA is the fraction responsible for PKR activation. We also found that p9-RNA induces the production of interferon-g (IFN-g), but not interleukin (IL-4) since only IFN-g gene promoter contains NF-B binding site. This study provides the first evidence that transcriptional control of gene expression by regulatory RNAs can be mediated by PKR through NF-B activation. A model for the mechanism of action of poly A(+) p9-RNA is proposed.
ISSN:0300-8177
1573-4919
DOI:10.1023/A:1024107512419