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. Author manuscript; available in PMC: 2018 Feb 13.
Published in final edited form as: Biochem J. 2016 Apr 12;473(12):1759–1768. doi: 10.1042/BCJ20160270

Figure 2. Abrogation of CARD14 inhibitory LR activity by deletion or psoriasis mutation induces BCL10 association.

Figure 2

(A, B) HaCaT keratinocytes were co-transfected with FLAG-CARD14 (0.125–0.2 μg), pNFκB-Luc and pRL-TK plasmids. NF-κB activity was determined as in Figure 1(D) (mean ± S.E.M. of three independent experiments). Representative expression of FLAG-CARD14 and tubulin in corresponding lysates was determined by immunoblotting. Significance determined by−two-way ANOVA. FC; fold change. (C) FC NF-κB activation of mutant compared with WT CARD14, in the presence or absence of the LR (calculated from data in A and B). Mean ± S.E.M. of three independent experiments. Significance determined by t test. (D) HEK293 cells were co-transfected with vectors encoding the indicated V5-CARD14 variants (0.1–1 μg) and FLAG-BCL10 (0.6–0.8 μg). Anti-FLAG immunoprecipitates were immunoblotted with the indicated antibodies. Representative of three independent experiments.