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. 2018 Jan 30;9:430. doi: 10.1038/s41467-018-02897-7

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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. 9 — Gimap5 is a critical regulator of GSK3β during T cell activation. Gimap5 controls regulation of GSK3β in T cells through vesicular sequestration and affects both the (1) (early) transcriptional program required for T cell growth, and (2) the late stage nuclear accumulation of P-Ser389 GSK3β required for the DNA damage response during cycling. Gimap5-deficient CD4⁺ T cells, fail to inhibit GSK3β leading to a failed transcriptional program and increased DNA damage during T cells proliferation