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. 2021 Sep 4;100(3):351–372. doi: 10.1007/s00109-021-02131-w

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© The Author(s) 2021

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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — SAMHD1, its functions, and implications for AGS and cancer

Cellular functions of SAMHD1 and functional consequences for mutated/dysfunctional or downregulated SAMHD1 are depicted. Mutated SAMHD1 might lead to displacement of ssDNA into the cytoplasm, where it can be detected by intracellular DNA sensors like cGAS. cGAS then produces cyclic guanosine monophosphate-adenosine monophosphate (cGAMP) to activate STING which in turn activates interferon regulatory factor 3 (IRF3) and the NF-κB pathways through the kinases TANK-binding kinase 1 (TBK1) and IκB kinase (IKK), thus inducing an IFN response. Consequences of dysfunctional SAMHD1 on AGS and cancer are displayed in the lower part of the figure. Unclear relations and consequences are indicated by question marks. Image created with Servier Medical Art (https://smart.servier.com/)