Figure 5.

Proposed model for the function of Eng in HSC quiescence. During transplantation-induced stress (left panel), Eng enhances TGF-β signaling in HSCs, resulting in activation of canonical (SMADs) and noncanonical (TAK1/p38/MK2) pathways, which ultimately leads to regulation of genes that control the cell cycle, and inhibition of the proliferation of HSCs, which ultimately promotes the HSC return to quiescence. However, lack of Eng (right panel) results in decreased signaling of canonical and noncanonical TGF-β pathways, resulting in enhanced proliferation of HSCs and impaired HSC quiescence.