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. 2020 Mar 6;11:1251. doi: 10.1038/s41467-020-15109-y

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© The Author(s) 2020

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 — There are two routes to generate the intracellular cysteine in cells: one is the cystine import though SLC7A11 and the other one is the transsulfuration pathway. Under basal conditions, the cystine import plays the dominate role in the GSH precursor cysteine generation. When the cystine import is blocked by erastin, the DJ-1 preserved transsulfuration pathway still could provide essential cysteine synthesis (refer to DJ-1 high with ferroptotic stress). DJ-1 depletion can markedly inhibit GSH levels only when the cystine import is blocked (refer to DJ-1 low with ferroptotic stress). The DJ-1 KD distinctly decreases Hcy levels by impairing SAHH activity via enhancing its interaction with AHCYL1. Decreased level of Hcy subsequently causes the depletion of GSH and eventually enhances ferroptotic cell death.