Figure 4
Figure 4. The effects of Wnt, LiCL, and DKK-1 on the proliferation of Eμ-TCL1–induced tumor B cells. CD5+ tumor B cells were incubated with or without 75 ng/mL recombinant mouse Wnt3a, 100 ng/mL Wnt 5a, 100 ng/mL DKK-1, or 20 mM LiCl (KCl as the control) for 16, 24, 48, or 72 hours. (A) Wnt3a and Wnt5a do not significantly affect the proliferation of CD5+ tumor B cells from Eμ-TCL1 mice. (B) Tumor B cells proliferate in response to the GSK-3β inhibitor, LiCl, but not to identical concentrations of control KCl. DKK-1, a canonical pathway inhibitor that blocks Wnt binding to LRP5/6, had only minimal effects at a range of concentrations tested.

The effects of Wnt, LiCL, and DKK-1 on the proliferation of Eμ-TCL1–induced tumor B cells. CD5+ tumor B cells were incubated with or without 75 ng/mL recombinant mouse Wnt3a, 100 ng/mL Wnt 5a, 100 ng/mL DKK-1, or 20 mM LiCl (KCl as the control) for 16, 24, 48, or 72 hours. (A) Wnt3a and Wnt5a do not significantly affect the proliferation of CD5+ tumor B cells from Eμ-TCL1 mice. (B) Tumor B cells proliferate in response to the GSK-3β inhibitor, LiCl, but not to identical concentrations of control KCl. DKK-1, a canonical pathway inhibitor that blocks Wnt binding to LRP5/6, had only minimal effects at a range of concentrations tested.

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