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. Author manuscript; available in PMC: 2017 Apr 1.
Published in final edited form as: J Immunol. 2016 Feb 26;196(7):3032–3042. doi: 10.4049/jimmunol.1501654

Figure 6. ATM over-expression suppresses signal joining in SCID mouse fibroblasts and DNA-PKcs deficient murine ES cells.

Figure 6

A. Left panel. Immunoblot analyses for ATM, DNA-PKcs or Beta-Actin expression of 12-50 μg of whole cell extracts from wild type or SCID ear fibroblasts, or the murine SCID fibroblast cell strain, Sf19. Right panel. Recombination percentage of the signal joint substrate 289/RFP/CFP in Sf19 cells transiently expressing RAG proteins and either no DNA-PKcs, human or mouse, wild type or mutant DNA-PKcs (vector, hwt, mwt, hD3922>A, mD3922>A,), 53BP1 or ATM. Cells were analyzed by flow cytometry as in Fig. 1. B. Left panel. Immunoblot analyses for ATM, DNA-PKcs or Beta-Actin expression of 50 μg whole cell extracts from wild type mouse fibroblasts, and wild type or DNA-PKcs deficient murine ES cells strains. Right panel. Recombination percentage of the signal joint substrate pJH201 or coding joint substrate pJH290 in DNA-PKcs deficient murine ES cells transiently expressing RAG proteins and varying levels of ATM, vector control, or DNA-PKcs as indicated. C. Proposed model. SEC structure is based on studies of Ru et al. (77).