Figure 7.

ERK-Dependent Phosphorylation of MEK1 T292 Feeds Back on AKT/mTORC1/FOXO3A Signaling to Balance HSC Quiescence and Differentiation

Effect of lentiviral expression of MEK1 and FOXO3A (wild-type or phosphosite mutants) and of PINK1 on mouse F/F and cKO HSCs or on iMEK-treated human HSCs.

(A–C) CFUs (A), ROS levels and Δψ per mitochondrial mass (B), and intracellular signaling (C) were determined after 6 weeks. Data show fold change relative to mouse cKO or human iMEK-treated HSCs (normalized as 1; dotted line; n = 3). Error bars represent the SD of the mean. ^∗p < 0.05, ^∗∗p < 0.01, and ^∗∗∗p < 0.001, comparing vector-infected HSCs with HSCs infected with the indicated constructs.

(D) Model: differentiation-promoting events in red; see text for details.