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. 2019 May 3;37(7):937–947. doi: 10.1002/stem.3015

Figure 2.

Figure 2

p53‐Dependent suppression of glycolysis in Fanconi anemia (FA) hematopoietic stem cells (HSCs). (A): Increased p53 and TP53‐induced glycolysis regulator (TIGAR) proteins in FA HSPCs. Whole‐cell lysates were extracted from 30,000 Lineage−Sca‐1+c‐kit+ isolated from wild‐type (WT), Fanca −/−, p53 −/−, or p53 −/− Fanca −/− mice followed by immunoblotting using antibodies against p53, TIGAR, or β‐actin. (B): Deletion of p53 increases F2,6BP level in Fanca −/− HSCs. SLAM cells isolated from WT, Fanca −/−, p53 −/−, or p53 −/− Fanca −/− mice were subjected to MicroAssay for F26BP. (C, D): Deletion of p53 increases glucose consumption and lactate production in FA HSCs. SLAM cells isolated from WT, Fanca −/−, p53 −/−, or p53 −/− Fanca −/− mice were subjected to glucose uptake (C) and lactate production analysis (D). Results depicted in (B)–(D) are means ± SD of three independent experiments (n = 6–9 per group); *, p < .05; **, p < .01.