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. 2007 May 10;117(6):1550–1557. doi: 10.1172/JCI31023

Figure 7. C76R mTACI dominantly interferes with signaling, but not ligand binding, by WT mTACI.

Figure 7

(A) 293T cells were transfected with 0.1 μg WT mTACI alone, 0.1 μg C76R mTACI, or 0.1 μg of each along with 0.1 μg of NF-κB–luc reporter plasmid and 10 ng control pRL-TK plasmid. Equal amounts of DNA were used for each transfection by using empty vector DNA when needed. After 4 hours, recombinant mBAFF (0.1 μg/ml) was added, and reporter gene activity was determined 20 hours later. NF-κB luciferase induction was normalized to Renilla luciferase intensity and total protein of each sample. Fold induction was calculated by dividing the normalized NF-κB luciferase result of BAFF-treated samples by the NF-κB luciferase result of untreated samples. n = 7. (B) The same assay as described in A was performed, with C76R mTACI that lacked the CRD1 domain (DM) substituting for C76R mTACI. Values represent the fold increase by BAFF stimulation compared with unstimulated sample and are the mean ± SEM from 6 independent experiments. (C) TACI surface expression and rhBAFF binding by 293T cells transfected with 1 μg of WT mTACI, 1 μg of C76R mTACI alone, or 1 μg of each.