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. 2018 Aug 17;9:3292. doi: 10.1038/s41467-018-05228-y

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© The Author(s) 2018

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — The STING hypothesis: activation of the innate immune system by DNA repair deficiencies in a DNA repair-deficient tumor cell. Cytosolic double-stranded DNA can be detected by cGAS which subsequently produces cGAMP (a cyclic dinucleotide), which in turn activates STING¹¹⁹. Upon activation, STING undergoes a conformational change, complexes with TANK-binding kinase 1 (TBK1) and relocates to peri-nuclear region. There, TBK1 phosphorylates IRF3 and NFKB, which translocate to the nucleus and lead to the expression of immune-related genes, including type I interferons¹²⁰