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Protein kinase R-dependent regulation of interleukin-10 in response to double-stranded RNA

  1. Author:
    Chakrabarti, A.
    Sadler, A. J.
    Kar, N.
    Young, H. A.
    Silverman, R. H.
    Williams, B.

  2. Author Address

    Sadler, Anthony J.; Williams, Bryan R. G.] Monash Univ, Monash Med Ctr, Monash Inst Med Res, Clayton, Vic 3168, Australia. [Chakrabarti, Arindam, Kar, Niladri, Silverman, Robert H.] Cleveland Clin, Lerner Res Inst, Dept Canc Biol, Cleveland, OH 44195 USA. [Kar, Niladri] Cleveland Clin, Lerner Res Inst, Dept Mol Cardiol, Cleveland, OH 44195 USA. [Young, Howard A.] NCI, Expt Immunol Lab, NIH, Frederick, MD 21702 USA.
    1. Year: 2008
  2. Journal: Journal of Biological Chemistry
    1. 283
    2. 37
    3. Pages: 25132-25139
  4. Type of Article: Article
  1. Abstract:

    The double-stranded RNA-activated protein kinase R (PKR) is an important component of antiviral defense. PKR participates in different signaling pathways in response to various stimuli to regulate translation via phosphorylation of the eukaryotic initiation factor 2 alpha, and transcription via activating NF-kappa B and IRF-1, to induce pro-inflammatory cytokines. Here we show PKR regulates interleukin-10 induction in response to double-stranded RNA, bacterial lipopolysaccaride, and Sendai virus infection. Using chemical inhibitors, dominant negative constructs, and genetic knockouts, we demonstrate that the PKR-mediated interleukin-10 induction engages JNK and NF-kappa B. Together, our data demonstrate the role of PKR in regulating an anti-inflammatory cytokine. The findings have significance in antiviral as well as broader innate immune responses.

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External Sources

  1. PMID: 18625702

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  1. No notes added.
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