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Fig. 5. In cells lacking STAT-1, overexpression of MDC1 restores ATM-dependent phosphorylation, which requires the FHA domain. (A) U3A cells were transfected with GFP control, wild-type GFP-MDC1 (WT) or a mutant GFP-MDC1- ${Delta}$ FHA ( ${Delta}$ FHA), lacking the FHA domain. Cells were immunoblotted with antibodies against the proteins indicated. (B,C) Effect of increasing amounts of (B) wild type (MDC1-WT) or (C) mutant (MDC1- ${Delta}$ FHA) on ATM-dependent phosphorylation as assessed by immunoblotting with antibodies against the proteins indicated. (D) Quantification of the Chk2^-T68 phosphorylation shown in B and C by densitometry. Data represent three independent experiments. (E) MEF STAT-1^–/– cells were transfected with GFP control, wild-type GFP-MDC1 (WT) or a mutant GFP-MDC1- ${Delta}$ FHA ( ${Delta}$ FHA). Cells were immunoblotted with an antibody against phosphorylated p53^-S15, p53 and actin (control). (F) MDC1 RNAi reduces expression of endogenous MDC1 in 2fTGH cells. (G) Transfection of MDC1 RNAi in 2fTGH cells reduced ATM-dependent phosphorylation following ${gamma}$ -IR (5 Gy) as assessed by immunoblotting with antibodies against the proteins indicated.

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