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. 2016 Oct 17;213(11):2383–2398. doi: 10.1084/jem.20160438

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© 2016 Bao et al.

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Figure 7. — The NFAT homology domain and DNA-binding domain of NFATC3 are required to enhance IRF7 activity. (A) HEK-293T cells were transfected with Myc-tagged IRF7 or truncated IRF7 and HA-tagged NFATC3 plasmids; 36 h after transfection, cell lysates were immunoprecipitated (IP) with anti-Myc beads, and then the immunoprecipitates and lysates were analyzed with anti-HA or anti-Myc antibodies. Scheme represents the IRF7 domain structure. (B) HEK-293T cells were transfected with HA-tagged NFATC3 or truncated NFATC3 and Myc-tagged IRF7 plasmids; cell lysates were immunoprecipitated with anti-Myc beads, and then the immunoprecipitates and lysates were analyzed with anti-HA or anti-Myc antibodies. Scheme represents the NFATC3 domain structure. (C) HEK-293T cells were transfected with 100 ng IFN-α4 luciferase reporter plasmid, 0.5 ng IRF7 expression vector, and 100 ng of full-length NFATC3 or truncated NFATC3 expression vectors. 0.1 ng renilla luciferase reporter plasmid was transfected simultaneously as an internal control. Results are presented as fold induction relative to the activity of renilla luciferase. Data are representative of four independent experiments.