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. 2008 Mar 1;22(5):587–600. doi: 10.1101/gad.1627708

Figure 5.

Figure 5.

Cep164 is an in vivo substrate of ATR. (A) Phosphorylation of Cep164 in cells expressing ATRKD. Cells with tetracycline-regulated ATRKD expression vector were grown in the presence or absence of doxycycline for 72 h. Cells were harvested at different time points after UV irradiation. Lysates were analyzed using immunoblotting. (B) Phosphorylation of Cep164 in cells with ATR knockdown. HeLa cells were transfected with either ATRi or GFPi and were irradiated with 20 J/M2 of UV 72 h post-transfection. Lysates were prepared at the indicated time points and analyzed using Western blotting. (C) UV-induced phosphorylation of Cep164 in AT cells. AT lymphoblastoid cells and ATM-complemented cells were irradiated with 20 J/M2 and lysed at the indicated time points. Cell lysates were analyzed as described. (D) IR-induced phosphorylation of Cep164 in cells with ATR knockdown. HeLa cells were transfected with either ATRi or GFPi; cells were irradiated with 20 Gy of IR 72 h post-transfection. Cell lysates were analyzed using Western blotting. (E) IR-induced phosphorylation of Cep164 in AT cells. AT lymphoblastoid cells and ATM-complemented cells were irradiated with 20 Gy of IR. Cell lysates were analyzed using Western blotting. (F) ATR kinase activity and Cep164 foci. HeLa cells were knocked down with GFP RNAi or ATRIP RNAi, and the cells were irradiated with IR or UV. The cells were subjected to immunostaining with ATRIP and Cep164 antibody.