Figure 3.
Clec12a KO NUP98::NSD1+NRASG12D cells demonstrate less proliferation kinetics in vitro. (A) Proliferation of Clec12a WT and KO NUP98::NSD1+NRASG12D cells in 12 days (mean ± SEM). (B) Growth of dTomato+ sgRNA-transduced and -untransduced cells over time in the proliferation assay (mean ± SEM). (C) Cumulative CFC yield is revealed for an initial plating of 1000 Clec12a WT and KO NRASG12D+NUP98::NSD1 transduced cells (mean ± SEM). (D) Frequency of cell cycle phases in Clec12a WT and KO NUP98::NSD1+NRASG12D cells (mean ± SEM). Cells were gated on dTomato+ cells, which correspond to Clec12a KO cells. (E) Proportion of apoptosis in Clec12a WT and KO NUP98::NSD1+NRASG12D cells (mean ± SEM). (F) Representative Wright-Giemsa–stained cytospin preparations of Clec12a WT and KO NUP98::NSD1+NRASG12D-transduced mouse BM cells (1000×). CFC, colony-forming cell; KO, knockout.

Clec12a KO NUP98::NSD1+NRASG12D cells demonstrate less proliferation kinetics in vitro. (A) Proliferation of Clec12a WT and KO NUP98::NSD1+NRASG12D cells in 12 days (mean ± SEM). (B) Growth of dTomato+ sgRNA-transduced and -untransduced cells over time in the proliferation assay (mean ± SEM). (C) Cumulative CFC yield is revealed for an initial plating of 1000 Clec12a WT and KO NRASG12D+NUP98::NSD1 transduced cells (mean ± SEM). (D) Frequency of cell cycle phases in Clec12a WT and KO NUP98::NSD1+NRASG12D cells (mean ± SEM). Cells were gated on dTomato+ cells, which correspond to Clec12a KO cells. (E) Proportion of apoptosis in Clec12a WT and KO NUP98::NSD1+NRASG12D cells (mean ± SEM). (F) Representative Wright-Giemsa–stained cytospin preparations of Clec12a WT and KO NUP98::NSD1+NRASG12D-transduced mouse BM cells (1000×). CFC, colony-forming cell; KO, knockout.

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