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TRIM32-TAX1BP1-dependent selective autophagic degradation of TRIF negatively regulates TLR3/4-mediated innate immune responses

Fig 7

TRIM32 links TRIF and TAX1BP1 through distinct domains.

(A-B) Effects of TRIM32 on colocalization of TRIF, TAX1BP1 and LC3 or LAMP1. HEK293 cells were transfected with the indicated plasmids for 20 hours, and then were fixed with 4% paraformaldehyde and subjected for confocal microscopy. (C) Effects of TRIM32-deficiency on poly(I:C)-induced TRIF-TAX1BP1 association. TRIM32+/+ and TRIM32-/- MLFs were left untreated or treated with poly(I:C) (50 μg/mL) for the indicated times before coimmunoprecipitation and immunoblotting analysis with the indicated antibodies. (D) Interactions of TRIM32 mutants with TAX1BP1 and TRIF. HEK293 cells were transfected with the indicated plasmids before coimmunoprecipitation and immunoblotting analysis with the indicated antibodies. (E) Interactions of TRIF mutants with TRIM32 and TAX1BP1. The experiments were similar performed as in (D). (F) A schematic presentation of interactions among TRIF, TRIM32 and TAX1BP1. (G) A model on the role of TRIM32 in regulation of TLR3/4-mediated signaling.

Fig 7

doi: https://doi.org/10.1371/journal.ppat.1006600.g007