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. 2015 May 7;10(5):e0126088. doi: 10.1371/journal.pone.0126088

Fig 8. ATM kinase activity mediates maximal reactivation of the EBV lytic cycle in Burkitt lymphoma cells.

Fig 8

(A) Cell lysates from Raji (A: i) and HH514-16 cells (A: ii) untreated or treated with camptothecin (CAMPTO), in the presence or absence of KU55933, were analyzed by immunoblots with antibodies against γH2AX (S135) and GAPDH; fold induction of γH2AX normalized to unphosphorylated H2AX are shown. (B) Cell lysates of Raji cells untreated, or treated with TPA, in the presence or absence of KU55933, were analyzed by immunoblots with antibodies against EA-D and GAPDH (B: i), ZEBRA and β-Actin (B: ii), and γH2AX (S135) and GAPDH (B: iii); The fold stimulation values of EA-D and ZEBRA normalized to GAPDH or γH2AX normalized to unphosphorylated H2AX are shown. The average fold-induction of EA-D normalized to GAPDH was determined (n = 3); ** denotes P<0.01; P = 0.00013 for TPA+KU55933 versus TPA (B: iv). (C) Cell lysates of HH514-16 cells untreated, or treated with AZA, in the presence or absence of KU55933, were analyzed by immunoblots with antibodies against EA-D and GAPDH (C: i) and ZEBRA, γH2AX, and β-Actin (C: ii); The fold stimulation values of EA-D, ZEBRA, and γH2AX are shown. The average fold-induction of EA-D normalized to GAPDH was determined (n = 3). ** denotes P<0.01; P = 0.00020 for AZA+KU55933 versus AZA (C: iii).