Figure 8
The diagram of control mechanisms for the functions of P18 on hematopoiesis. The RUNX1b overexpression can upregulate TGF-β signaling and P18, and the inhibition of TGF-β signaling can restore the expression level of P18. The P18 overexpression at D0 can severely decrease the product of CD34highCD43− cells and their derived populations but not CD34lowCD43− cells that can only be blocked by RUNX1b overexpression at D0. The P18 overexpression at D10 can significantly increase the product of classic hematopoietic populations, which can be counteracted by the inhibition of NF-κB signaling. P18 has distinctive function on hematopoietic differentiation at different stage, which are both related to the change of cell cycle status.
