Beyond autophagy: New roles for ULK1 in immune signaling and interferon responses

Diana Saleiro*, Ewa M. Kosciuczuk, Leonidas C. Platanias

*Corresponding author for this work

Research output: Contribution to journalShort surveypeer-review

9 Scopus citations

Abstract

The human serine/threonine kinase ULK1 is the human homolog of the Caenorhabditis elegans Unc-51 kinase and of the Saccharomyces cerevisiae autophagy-related protein kinase Atg1. As Unc-51 and Atg1, ULK1 regulates both axon growth and autophagy, respectively, in mammalian cells. However, a novel immunoregulatory role of ULK1 has been recently described. This kinase was shown to be required for regulation of both type I interferon (IFN) production and induction of type I IFN signaling. Optimal regulation of IFN production is crucial for generation of effective IFN-immune responses, and defects in such networks can be detrimental for the host leading to uncontrolled pathogen infection, tumor growth, or autoimmune diseases. Thus, ULK1 plays a central role in IFN-dependent immunity. Here we review the diverse roles of ULK1, with special focus on its importance to type I IFN signaling, and highlight important future study questions.

Original languageEnglish (US)
Pages (from-to)17-22
Number of pages6
JournalCytokine and Growth Factor Reviews
Volume29
DOIs
StatePublished - Jun 1 2016

Keywords

  • Immune signaling
  • Innate immunity
  • Interferon
  • Signal transduction
  • ULK1

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Immunology and Allergy
  • Immunology
  • Biochemistry, Genetics and Molecular Biology(all)

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