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. 2022 Nov 26;13:7281. doi: 10.1038/s41467-022-34871-9

Fig. 5. IKKβ acts as the convergence point for inflammatory signals to cause ARID1A destruction.

Fig. 5

a IB analysis of C4-2 cells treated with TNFα, IL-6 and IFN-γ for the indicated duration of time. b IB analysis of C4-2 cells stimulated with TNFα with or without MG132 treatment for the indicated duration of time. c IB analysis of C4-2 cells transfected with scramble or P50, P52, or P65 oligonucleotides with or without TNFα treatment. d IB analysis of C4-2 cells transfected with scramble or IKKβ and IKKα oligonucleotides with or without TNFα treatment. e IB analysis of the WCL from WT and IKKβ KD C4-2 cells with or without TNFα treatment and anti-ARID1A immunoprecipitates as indicated. f IB analyses of the WCL and anti-ARID1A immunoprecipitates of C4-2 cells. g IB analysis of nuclear extracts from C4-2 cells after gel-filtration fractionation. Cells were treated with 20 ng/ml TNFα for 30 min before harvesting. h IB analysis of the indicated proteins in C4-2 control and IKKβ KD cells with or without IKKβ-WT, IKKβ-SA or IKKβ-SD overexpression. i IB analysis of C4-2 cells treated with IL-1β or c-GAMP for the indicated duration of time. All experiments were repeated three times independently with similar results; data from one representative experiment are shown. Source data are provided as a Source Data file.