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. 2013 Oct;15(10):1342–1352. doi: 10.1093/neuonc/not077

Fig. 4.

Fig. 4.

Silencing of ATAD3A attenuated DNA repairs before and after irradiation. (A, B) Comparison of the average γ-H2AX foci number (red fluorescence) between wild-type and T98G/ATAD3Akd cells before and after 6-Gy radiation. Prior to 6-Gy radiation treatment, the number of γ-H2AX foci was marginally reduced in T98G/ATAD3Akd cells and was significantly decreased 1 h postirradiation compared with wild-type cells, ***P < .001. (C) Gel electrophoresis assay for DSBs. Compared with control and vector-transfected cells, DNA DSBs were more frequent in ATAD3Akd T98G cells prior to radiation. Four hours postradiation (6 Gy), DSBs remained evident in T98G/ATAD3Akd cells, whereas those in the control and vector-transfected cells were mostly mended. (D) Immunoblotting of whole cell and nuclear protein extraction of wild-type and T98G/ATAD3Akd cells. Attenuated γ-H2AX was evident in T98G/ATAD3Akd cells before and after radiation treatment. Autophosphorylation of ATM on Ser1981 in response to irradiation was diminished in T98G/ATAD3Akd cells, as well as ATM and NBS1 compared with those in the wild-type T98G cells, indicating that DNA repairs might be affected. Chk2, checkpoint kinase 2.