Functionally distinct effects of the C-terminal regions of IKKε and TBK1 on type I IFN production

PLoS One. 2014 Apr 10;9(4):e94999. doi: 10.1371/journal.pone.0094999. eCollection 2014.

Abstract

Inhibitor of κB kinase ε (IKKε) and TANK binding kinase 1 (TBK1), so-called non-canonical IKKs or IKK-related kinases, are involved in the cellular innate immunity by inducing type I IFNs. Two kinases commonly phosphorylate transcription factors IRF3 and IRF7 in type I IFN production pathway. In contrast to TBK1, underlying mechanisms of IKKε activation and regions required for activation of downstream molecules are poorly understood. In this study, we investigated regions of IKKε required for the activation of type I IFN promoter specially, by focusing on the C-terminal region. To show the functional significance of the IKKε C-terminal region on type I IFN production, we employed various mutant forms of IKKε and compared to corresponding region of TBK1. We identified the specific regions and residues of IKKε involved in the activation of downstream signaling. Interestingly, corresponding region and residues are not required for activation of downstream signaling by TBK1. The results highlight the importance of the C-terminal region in the functional activity of IKKε in innate immune response and also the difference in activation mechanisms between IKKε and the closely related TBK1.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • HEK293 Cells
  • Humans
  • I-kappa B Kinase / genetics
  • I-kappa B Kinase / metabolism*
  • Interferon Type I / genetics
  • Interferon Type I / metabolism*
  • L Cells
  • Mice
  • Phosphorylation
  • Promoter Regions, Genetic
  • Protein Serine-Threonine Kinases / genetics
  • Protein Serine-Threonine Kinases / metabolism*
  • Signal Transduction / physiology*

Substances

  • Interferon Type I
  • Protein Serine-Threonine Kinases
  • TBK1 protein, human
  • I-kappa B Kinase

Grants and funding

This research was supported in part by Grant–in-Aid 25460582 for Scientific Research (C) from the Ministry of Education, Culture, Sports, Science and Technology of Japan, to TK. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. No additional external funding was received for this study.