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. 2015 Jan 21;89(7):3804–3818. doi: 10.1128/JVI.02959-14

Fig 5.

Fig 5

Tom70, Hsp90, and IRF3 form a dynamic complex during Sendai virus-induced apoptosis. (A, B, E, and G) HEK293T cells were transfected with the indicated constructs for 36 h and then subjected to immunoprecipitation with anti-HA antibody. The immunoprecipitates were analyzed by immunoblotting with the indicated antibodies. TM, transmembrane domain. (C) The interactions between Tom70 and Hsp90 were tested by the oblique-incidence reflectivity difference method. (D) HEK293 cells were transfected with the indicated plasmids for 24 h and then infected with SeV for the indicated times. Cell lysates were analyzed by immunoblotting with the indicated antibodies. (F) HEK293 cells were first transfected with NC or Tom70 siRNA and then rescued with the indicated siRNA-resistant Tom70 constructs. Cell lysates were collected for Western blot analysis with the indicated antibodies. (H) HEK293 cells were first transfected with NC or Hsp90 siRNA and then rescued with the indicated siRNA-resistant Hsp90 constructs. Cell lysates were collected for Western blot analysis with the indicated antibodies. NC, nonspecific control siRNA; R192A, K195A, rTom70, rR192A, and rK195A, point mutants of Tom70; M2, M4, rHsp90, rM2, and rM4, point mutants of Hsp90.