Figure 2.
Figure 2. Mad1 and p27Kip1 are essential for RARα-mediated inhibition of CFU proliferation. Whole bone marrow of each genotype was plated at 5 × 104 cells/mL in methylcellulose supplemented with FCS, SCF, erythropoietin (Epo), IL-3, and IL-6. Ligands were added directly to the semisolid cultures. Cells were cultured for 7 days and then counted (colony defined as > 50 cells). indicates control; and ▪, retinoid. (A) Colony formation in the presence of ATRA (10–6 M). Data are expressed as percent colonies of control ± SEM (ethanol-treated culture for each genotype). (B) Colony formation in the presence of an RARα-selective agonist (AGN195183, 10–6 M). (C) Colony formation in the presence of an RARβ/γ-selective agonist activity (ATRA and the RARα-specific antagonist AGN194301; 10–6 M). n ≥ 4 for all genotype/ligand combinations. **P ≤ .003.

Mad1 and p27Kip1 are essential for RARα-mediated inhibition of CFU proliferation. Whole bone marrow of each genotype was plated at 5 × 104 cells/mL in methylcellulose supplemented with FCS, SCF, erythropoietin (Epo), IL-3, and IL-6. Ligands were added directly to the semisolid cultures. Cells were cultured for 7 days and then counted (colony defined as > 50 cells). indicates control; and ▪, retinoid. (A) Colony formation in the presence of ATRA (10–6 M). Data are expressed as percent colonies of control ± SEM (ethanol-treated culture for each genotype). (B) Colony formation in the presence of an RARα-selective agonist (AGN195183, 10–6 M). (C) Colony formation in the presence of an RARβ/γ-selective agonist activity (ATRA and the RARα-specific antagonist AGN194301; 10–6 M). n ≥ 4 for all genotype/ligand combinations. **P ≤ .003.

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