Figure 2.
FOXP1 loss enhances HSPC oxidative stress. CD34+ HSPCs were isolated from healthy human CB samples and transduced with the indicated GFP- and shRNA-encoding lentiviral vectors directed against FOXP1 (#a, #b, and #c) or luciferase as a control (Ctl). After 3 days, FOXP1 (A; bottom) and NRF2 (B) protein expression was assessed using western blot; β-actin was used as a loading control; size markers (kDa) are indicated on the left (1 representative experiment; n ≥ 3); (A [top],C) O2.− levels of total (−, untreated) or GFP+ cells were assessed using a DHE probe and flow cytometry in total CD34+ (A) (n = 7), and CD34+CD38+ and CD34+CD38− (C) (n = 3) cell populations. Data are expressed as MFI (a.u.); 1 spot represents 1 independent sample from independent experiments.

FOXP1 loss enhances HSPC oxidative stress. CD34+ HSPCs were isolated from healthy human CB samples and transduced with the indicated GFP- and shRNA-encoding lentiviral vectors directed against FOXP1 (#a, #b, and #c) or luciferase as a control (Ctl). After 3 days, FOXP1 (A; bottom) and NRF2 (B) protein expression was assessed using western blot; β-actin was used as a loading control; size markers (kDa) are indicated on the left (1 representative experiment; n ≥ 3); (A [top],C) O2.− levels of total (−, untreated) or GFP+ cells were assessed using a DHE probe and flow cytometry in total CD34+ (A) (n = 7), and CD34+CD38+ and CD34+CD38 (C) (n = 3) cell populations. Data are expressed as MFI (a.u.); 1 spot represents 1 independent sample from independent experiments.

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