AKT is involved in DMSR. (A) G1 cells were preincubated with AKT, CHK1, and CHK2 inhibitors for 1 h and then treated with IR. DMSR was determined in these cells 4 h after IR. Quantitation of microtubule length is shown (n > 50). (B) Western blot analysis showed the siAKT efficiency. (C) DMSR is inhibited by AKT depletion in G1 cells. Quantitation of microtubule length is shown (n > 50). (D) Semiquantitative analysis of relative NEDD1 or PCNT signal intensity at the centrosomes in G1 cells treated with scramble siRNA or siAKT is shown in box plot (n > 50). (E) Quantitative analysis of GFP-EB3 comet velocity in siRNA-treated live GFP-EB3–expressing G1 cells is shown in box plot (n > 30). (F) Quantitative analysis of relative centrosomal GFP-EB3 intensity in siRNA-treated live GFP-EB3–expressing G1 RPE-1 cells is shown in box plot (n > 30). (G) IR treatment led to the increase of pT308 AKT signal in the cytoplasmic fraction, but not in the nuclear fraction. (H) Kinetics of IR-induced pT308 AKT. The pT308 AKT signal in the cytoplasmic fraction was determined by Western blot in G1 cells at indicated time points after 2 Gy IR. (I) DNA-PK inhibitor treatment attenuated IR-induced pT308 AKT. The cytoplasmic pT308 AKT was examined by anti-pT308 AKT antibody. (J) The cytoplasmic IR-induced pT308 AKT was examined in G1 U2OS cells after PDK1 inhibitors BX-912 or BX-795 treatment. (K) G1 cells were pretreated with BX-912 for 1 h and exposed to 2 Gy IR. DMSR was measured by microtubule regrowth assay (n > 50). ****, P < 0.0001; **, P < 0.01; ns, not significant. A.U., arbitrary units; MT, microtubule; UT, untreated.