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. Author manuscript; available in PMC: 2009 Apr 14.
Published in final edited form as: Biochem Biophys Res Commun. 2006 Sep 28;350(4):866–871. doi: 10.1016/j.bbrc.2006.09.097

Figure 3. Gold compounds inhibit MyD88-dependent signaling pathways.

Figure 3

A-C) 293T cells were transfected with NF-κB binding site(2x)-luciferase reporter plasmid and the expression plasmid of (A) MyD88, (B) IKKβ, or (C) p65. After 24 hrs, cells were further treated with auranofin (5, 10 μM) or sodium tetrachloroaurate (20, 50 μM) for 6 hrs. Relative luciferase activity (RLA) was determined as described in the legend of Fig. 1. Values are mean±SEM (n=3). (A) **, Significantly different from MyD88 plus vehicle, p<0.01. (B) ++, Significantly different from IKκB plus vehicle, p<0.01. +, Significantly different from IKKβ plus vehicle, p<0.05. (C) ##, Significantly different from p65 plus vehicle, p<0.01. D) RAW264.7 cells were pretreated with auranofin (5, 10 μM) for 1 h and then stimulated with LPS (50 ng/ml) for 30 mins. Cell lysates were subjected to SDS-PAGE and probed with anti-IRAK-1 (upper) or anti-β-actin (lower) antibody. The panels are representative data from more than three independent experiments. Veh, vehicle; Au(I), auranofin; Au(III), sodium tetrachloroaurate dihydrate.