Figure 1.
Coinactivation of Hoxa9/β-catenin induces severe HSC defects. (A) Schematic representation of experimental procedures. Absolute number of HSPC populations (B) and percentage CD45.2+ donor cells (C) from indicated mice at 12 week time point (at least n = 3 mice/group). Floxed allele deletion was achieved by intraperitoneal injection of tamoxifen for 5 consecutive days. β-cateninfl/fl mice treated with corn oil (vehicle) served as WT control as indicated. (D) LTC-IC frequency from HSPCs as indicated. Enrichment in stem related gene sets (E) and gene ontology analysis (F) of LSKs isolated from mice that received transplant. All data represent mean ± standard error of the mean (SEM). P values calculated by t test. ∗P ≤ .05; ∗∗P ≤ .01; ∗∗∗P ≤ .001; ∗∗∗∗P ≤ .0001; NS, P > .05.

Coinactivation of Hoxa9/β-catenin induces severe HSC defects. (A) Schematic representation of experimental procedures. Absolute number of HSPC populations (B) and percentage CD45.2+ donor cells (C) from indicated mice at 12 week time point (at least n = 3 mice/group). Floxed allele deletion was achieved by intraperitoneal injection of tamoxifen for 5 consecutive days. β-cateninfl/fl mice treated with corn oil (vehicle) served as WT control as indicated. (D) LTC-IC frequency from HSPCs as indicated. Enrichment in stem related gene sets (E) and gene ontology analysis (F) of LSKs isolated from mice that received transplant. All data represent mean ± standard error of the mean (SEM). P values calculated by t test. ∗P ≤ .05; ∗∗P ≤ .01; ∗∗∗P ≤ .001; ∗∗∗∗P ≤ .0001; NS, P > .05.

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