Figure 10.

Filamin B accelerates type I IFN-induced apoptosis. (A) HeLa cells transfected with shRNAs or shControl were treated with IFNα. Cell lysates were immunoblotted with anti-TRAIL-R1, anti-PARP, anti-Xpress, or anti-β actin antibody. (B) HisMax-c-filamin B was expressed in M2 cells with or without Myc-dn-JNK1. After incubation with IFNα, cell lysates were subjected to immunoblot analysis. Mock indicates cells transfected with empty vectors. In A and B, the numerals indicate the ratio of quantified intensity of each band to that of β-actin, relative to that seen at the zero time of IFNα treatment, and they are representative of three independent experiments. (C) Binding of type I IFNs to their receptor (IFNR) induces the recruitment of filamin B to membrane ruffles and the binding of Rac1, MEKK1, MKK4, and JNK1 to filamin B scaffold. GEF, a putative guanine nucleotide exchange factor, may then specifically link IFN signal to Rac1 for the successive activation of downstream kinases and thereby for the generation of type I IFN-mediated biological responses, such as apoptosis.