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. 2020 Mar 2;39(15):3195–3205. doi: 10.1038/s41388-020-1209-4

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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. 3 — K562 ZBTB7A KO and control cells underwent transcriptional profiling, metabolic flux analysis, and 2DG treatment. a Gene set enrichment analysis from RNA-Seq data. b Expression of ENO2 (Enolase), SLC2A1, and SLC2A3 (glucose membrane transporters), PGM2 and PGM3 (phosphoglycerate mutases) measured by RNA-Seq. c ECAR following the addition of glucose, Rot/AA, and 2DG. d Glycolytic capacity calculated as the ECAR after electron transport chain inhibition. e Glycolytic reserve calculated as the difference between glycolysis after glucose infusion and glycolytic capacity (F) cell viability after 2DG treatment. *p value < 0.05 compared with control cells.