Michael Karin
University of California, San Diego, San Diego, CA, USA

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Publications (2)27.71 Total impact

  • Source
    Article: Transcriptional regulation of the Th17 immune response by IKKα
    Li Li, Qingguo Ruan, Brendan Hilliard, Jennifer DeVirgiliis, Michael Karin, Youhai H. Chen
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    ABSTRACT: Th17 cells are a subset of T cells that play crucial roles in the pathogenesis of many inflammatory diseases. We report here the identification of IKKα (inhibitor of NF-κB kinase-α) as a key transcriptional regulator of the Th17 lineage. T cells expressing a nonactivatable form of IKKα were significantly compromised in their ability to produce IL-17 and to initiate neural inflammation. IKKα is present in the nuclei of resting CD4+ T cells. Upon Th17 differentiation, IKKα selectively associated with the Il17a locus, and promoted its histone H3 phosphorylation and transcriptional activation in a NF-κB–independent manner. These findings indicate that nuclear IKKα maintains the Th17 phenotype by activating the Il17a gene.
    Journal of Experimental Medicine 04/2011; 208(4):787-796. · 13.85 Impact Factor
  • Source
    Article: Transcriptional regulation of the Th17 immune response by IKK(alpha).
    Li Li, Qingguo Ruan, Brendan Hilliard, Jennifer Devirgiliis, Michael Karin, Youhai H Chen
    [show abstract] [hide abstract]
    ABSTRACT: Th17 cells are a subset of T cells that play crucial roles in the pathogenesis of many inflammatory diseases. We report here the identification of IKKα (inhibitor of NF-κB kinase-α) as a key transcriptional regulator of the Th17 lineage. T cells expressing a nonactivatable form of IKKα were significantly compromised in their ability to produce IL-17 and to initiate neural inflammation. IKKα is present in the nuclei of resting CD4(+) T cells. Upon Th17 differentiation, IKKα selectively associated with the Il17a locus, and promoted its histone H3 phosphorylation and transcriptional activation in a NF-κB-independent manner. These findings indicate that nuclear IKKα maintains the Th17 phenotype by activating the Il17a gene.
    Journal of Experimental Medicine 03/2011; 208(4):787-96. · 13.85 Impact Factor

Institutions

  • 2011
    • University of California, San Diego
      • Department of Pharmacology
      San Diego, CA, USA
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