DC Field | Value | Language |
---|---|---|
dc.contributor.author | Kwon, Do Hyeong | ko |
dc.contributor.author | Sesaki, Hiromi | ko |
dc.contributor.author | Kang, Suk-Jo | ko |
dc.date.accessioned | 2018-06-16T06:38:36Z | - |
dc.date.available | 2018-06-16T06:38:36Z | - |
dc.date.created | 2018-05-28 | - |
dc.date.created | 2018-05-28 | - |
dc.date.issued | 2018-06 | - |
dc.identifier.citation | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.500, no.2, pp.497 - 503 | - |
dc.identifier.issn | 0006-291X | - |
dc.identifier.uri | http://hdl.handle.net/10203/242431 | - |
dc.description.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-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. | - |
dc.language | English | - |
dc.publisher | ACADEMIC PRESS INC ELSEVIER SCIENCE | - |
dc.subject | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject | NLRP3 INFLAMMASOME ACTIVATION | - |
dc.subject | INNATE IMMUNITY | - |
dc.subject | MITOCHONDRIAL FISSION | - |
dc.subject | ADAPTER | - |
dc.subject | PROTEIN | - |
dc.subject | TRANSLOCATION | - |
dc.subject | INFECTION | - |
dc.subject | KINASE | - |
dc.subject | PHOSPHORYLATION | - |
dc.title | Intracellular calcium is a rheostat for the STING signaling pathway | - |
dc.type | Article | - |
dc.identifier.wosid | 000431836700060 | - |
dc.identifier.scopusid | 2-s2.0-85045703826 | - |
dc.type.rims | ART | - |
dc.citation.volume | 500 | - |
dc.citation.issue | 2 | - |
dc.citation.beginningpage | 497 | - |
dc.citation.endingpage | 503 | - |
dc.citation.publicationname | BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | - |
dc.identifier.doi | 10.1016/j.bbrc.2018.04.117 | - |
dc.contributor.localauthor | Kang, Suk-Jo | - |
dc.contributor.nonIdAuthor | Sesaki, Hiromi | - |
dc.description.isOpenAccess | N | - |
dc.type.journalArticle | Article | - |
dc.subject.keywordAuthor | STING | - |
dc.subject.keywordAuthor | Mitochondria | - |
dc.subject.keywordAuthor | Calcium | - |
dc.subject.keywordAuthor | DRP1 | - |
dc.subject.keywordAuthor | Type I interferon | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | NLRP3 INFLAMMASOME ACTIVATION | - |
dc.subject.keywordPlus | INNATE IMMUNITY | - |
dc.subject.keywordPlus | MITOCHONDRIAL FISSION | - |
dc.subject.keywordPlus | ADAPTER | - |
dc.subject.keywordPlus | PROTEIN | - |
dc.subject.keywordPlus | TRANSLOCATION | - |
dc.subject.keywordPlus | INFECTION | - |
dc.subject.keywordPlus | KINASE | - |
dc.subject.keywordPlus | PHOSPHORYLATION | - |
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