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. 2020 Apr 2;295(20):7113–7125. doi: 10.1074/jbc.RA119.011895

Figure 1.

Figure 1.

Samd14 genetic complementation in Samd14–Enh−/− erythroid progenitor cells rescues SCF/c-Kit signaling. A, model depicting the Samd14–Enh requirement for induction of Samd14 expression upon anemia and Samd14-mediated promotion of c-Kit signaling (phosphorylation of AKT). In Samd14–Enh-deleted (Enh−/−) cells, pAKT levels are lower in response to SCF (4). B, phospho-flow cytometry quantitating pAKT levels in WT (n = 6) and Enh−/− (n = 6) over a 20-min (m) time course of SCF stimulation. C, experimental layout of spleen ex vivo retroviral infection and culture. D, representative Western blotting of WT and Enh−/− protein lysates infected with EV or full-length HA-tagged Samd14. E, flow cytometric analysis depicting the population of GFP+CD71+Kit+ cultured spleen erythroid progenitors. F, phospho-flow cytometry quantitating pAKT levels in infected WT (n = 6) and Enh−/− (n = 6) over a 20-min time course of SCF stimulation. Error bars represent the standard error of the mean (S.E.). *, p < 0.05; **, p < 0.01 (two-tailed unpaired Student's t test). FSC, forward scatter.