Figure 3.
Tifab deletion disrupts signaling pathways regulating LSPC function. (A-F) GSEA of RNA-seq data comparing WT and Tifab KO LSPCs. Tifab KO LSPCs exhibit downregulation of gene sets associated with OXPHOS (A), Myc targets (B), HOXA9 and MEIS1 signaling (C), MTORC1 signaling (D), KMT2A::MLLT3 fusion targets (E), and glycolysis (F), compared with WT LSPCs. (G) Quantitative polymerase chain reaction analysis of glycolysis-related enzyme expression in WT and Tifab KO LSPCs. Representative results from 3 independent experiments, each performed with 3 replicates. (H-I) Glucose uptake in WT and Tifab KO (n = 7) (H) or Con and TIFAB OE (n = 16) LSPCs (I). ∗P < .05; ∗∗P < .01. In panel G, Mann-Whitney U test was used; in panels H-I, Student t test was used. FDR, false discovery rate; NES, normalized enrichment score.

Tifab deletion disrupts signaling pathways regulating LSPC function. (A-F) GSEA of RNA-seq data comparing WT and Tifab KO LSPCs. Tifab KO LSPCs exhibit downregulation of gene sets associated with OXPHOS (A), Myc targets (B), HOXA9 and MEIS1 signaling (C), MTORC1 signaling (D), KMT2A::MLLT3 fusion targets (E), and glycolysis (F), compared with WT LSPCs. (G) Quantitative polymerase chain reaction analysis of glycolysis-related enzyme expression in WT and Tifab KO LSPCs. Representative results from 3 independent experiments, each performed with 3 replicates. (H-I) Glucose uptake in WT and Tifab KO (n = 7) (H) or Con and TIFAB OE (n = 16) LSPCs (I). ∗P < .05; ∗∗P < .01. In panel G, Mann-Whitney U test was used; in panels H-I, Student t test was used. FDR, false discovery rate; NES, normalized enrichment score.

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