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. 2019 Jan 22;10(2):57. doi: 10.1038/s41419-018-1283-5

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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. 8 — eIF5B (gray oval) promotes translation of XIAP, Bcl-xL, cIAP1, c-FLIP_S, and Nrf2 (green ovals). These, in turn, promote cell survival in the presence of TRAIL by abrogating the effects of reactive oxygen species (ROS) and/or the functions of FADD, caspase-9 (cas-9), and caspase-7 (cas-7). As XIAP, cIAP1, and Bcl-xL all act downstream of mitochondria, eIF5B might also promote resistance to intrinsic apoptosis—for instance, owing to DNA damage from chemotherapy or radiation treatment (represented by the lightning bolt)