Intracellular calcium is a rheostat for the STING signaling pathway

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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-beta production. We demonstrate that the mitochondria fission mediator DRP1 is crucial for ionomycin-induced inhibition of IFN-beta 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. (C) 2018 Elsevier Inc. All rights reserved.
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Issue Date
2018-06
Language
English
Article Type
Article
Keywords

ENDOPLASMIC-RETICULUM STRESS; NLRP3 INFLAMMASOME ACTIVATION; INNATE IMMUNITY; MITOCHONDRIAL FISSION; ADAPTER; PROTEIN; TRANSLOCATION; INFECTION; KINASE; PHOSPHORYLATION

Citation

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.500, no.2, pp.497 - 503

ISSN
0006-291X
DOI
10.1016/j.bbrc.2018.04.117
URI
http://hdl.handle.net/10203/242431
Appears in Collection
BS-Journal Papers(저널논문)
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