Fig. 3: HSV1 (FmutRHIM) infection activates MLKL and drives ZBP1-RIPK3 complex formation. | Cell Death & Disease

Fig. 3: HSV1 (FmutRHIM) infection activates MLKL and drives ZBP1-RIPK3 complex formation.

From: Species-independent contribution of ZBP1/DAI/DLM-1-triggered necroptosis in host defense against HSV1

Fig. 3

a, b IB analysis to detect p-MLKL, total MLKL, ZBP1, ICP0, and β-actin from WT MEFs (a) or SVEC4-10 (b) infected with HSV1 (F) or HSV1 (FmutRHIM) for the indicated times. c Immunoprecipitation (IP) analysis to detect the interaction of ZBP1 and RIPK3 in SVEC4-10 cells. Wild-type SVEC4-10 cells were infected with HSV1 (FmutRHIM), mock infected cells as the control. ZBP1-deficient SVEC4-10 cells infected with the same amount HSV1 (FmutRHIM) were also employed as a control. RIPK3 were immunoprecipitated, and ZBP1, RIPK3, and MLKL were analyzed by IB. Whole-cell extract (5% input) was examined in parallel for RIPK3, ZBP1, MLKL, and HSV1 proteins-ICP0. Black solid triangle represents F, hollow triangle represents FmutRHIM, and solid circular represents mock. d Kinetics of cell death of type I interferon receptor (IFNAR)-deficient MEFs infected with HSV1 (F) or HSV1 (FmutRHIM). See also Supplementary Figure 2

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