Intracellular calcium is a rheostat for the STING signaling pathway

Dohyeong Kwon, Hiromi Sesaki, Suk Jo Kang

Research output: Contribution to journalArticlepeer-review

Abstract

Stimulator of IFN genes (STING) is essential for the DNA-sensing innate immune pathway. Recently, evidence is emerging that suggests STING also plays important roles in autoimmunity, cancer therapy, and senescence. Although a multitude of post-translational modifications that regulate the STING pathway have been discovered, the cellular events that guide STING translocation remain unclear. Here, we show, paradoxically, that both BAPTA-AM-mediated calcium depletion and ionomycin-induced calcium elevation suppress STING translocation and STING-mediated IFN-β production. We demonstrate that the mitochondria fission mediator DRP1 is crucial for ionomycin-induced inhibition of IFN-β production. Furthermore, knockout of DRP1 suppressed ionomycin-induced increases in calcium as well as mitochondrial fragmentation. Collectively, our findings reveal that the induction of STING signaling is contingent on a fine-tuning of intracellular calcium levels.

Original languageEnglish (US)
Pages (from-to)497-503
Number of pages7
JournalBiochemical and Biophysical Research Communications
Volume500
Issue number2
DOIs
StatePublished - Jun 2 2018

Keywords

  • Calcium
  • DRP1
  • Mitochondria
  • STING
  • Type I interferon

ASJC Scopus subject areas

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

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