Fig. 5

Both ADAR1 isoforms (p150 and p110), independently of their active deaminase domains, modulate CDK2 and rescue cell proliferation in shMETTL3 cells. a shADAR1 U87MG cells (with the shRNA targeting the 3′UTR of the endogenous ADAR1) were transfected with the active and the inactive (E/A) ADAR1 constructs (either p150 or p110) and cell proliferation (MTS assay) was tested at 72 and 96 h pt. b Western blotting analysis of ADAR1 and CDK2 proteins of the same cells at 72 h pt. are shown. c, d Cell proliferation (MTS assay) of shADAR1 U87MG cells transfected with ADAR1 p110 vector carrying an inactive RNA-binding domains (RBDs-mut) and western blotting analysis of ADAR1 and CDK2 proteins (72 h pt) is shown. e Cartoon showing the rescue experiment in shMETTL3 U87MG cells transfected with either ADAR1 (red), ADAR1 E/A (blue), empty vector (gray line), and untransfected cells (black line). On the left, a control western blotting analysis 72 h pt. showing that ADAR1 active and inactive were overexpressed at similar levels. GAPDH was used as control; on the right, the same cells were tested for cell proliferation (48–72 h pt). Values are represented as means ± SD, *p ≤ 0.05, **p ≤ 0.01, ***p ≤ 0.001