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. 2019 Jul 17;10:3143. doi: 10.1038/s41467-019-11048-5

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© The Author(s) 2019

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. 7 — Model of innate immune response activation in BRCA2-deficient cells. Intrinsic replication stress and unrepaired DSBs cause genomic instability leading to release of DNA into the cytosol. Cytosolic DNA assembles into micronuclei, where it binds to and activates cyclic GMP-AMP synthase (cGAS), a cytosolic DNA sensor. cGAS catalyzes the synthesis of cyclic GMP-AMP (cGAMP), which binds to and activates STING (stimulator of interferon genes). STING promotes TBK1-dependent phosphorylation of interferon response factor 3 (IRF3), which translocates into the nucleus as a homodimer to induce transcription of type I interferon. Secreted interferon binds to transmembrane receptors and elicits autocrine and paracrine signaling, both mediated by the JAK-STAT pathway. Janus kinases (JAKs) phosphorylate signal transducer and activator of transcription 1 (STAT1) and 2 (STAT2), which enter the nucleus as a heterodimer to initiate transcription of interferon-stimulated genes (ISGs). ER, endoplasmic reticulum